Fermented dairy products are known for their efficiency in delivering and protecting probiotic microorganisms. However, there is a growing demand for diversification of the market with plant-based products. The aim of this study was to develop an oat beverage enriched with inulin and fermented with Lacticaseibacillus rhamnosus LR B and evaluate its synbiotic effects in vitro. For this purpose, the validated dynamic colon model (the TNO Intestinal Model TIM-2) was used with focus on the composition of the gut microbiota and its production of metabolites to evaluate the functionality. The fermentation kinetics, sugars, organic acids and inulin dosage in the fermented oat beverage were also evaluated. The acidification rate was 16.91 10-3 pH units.min-1, reaching the final pH of 4.5 in 2.38 ± 0.05 h. Dosages of sucrose, glucose and lactic acid were 23.35 ± 0.45 g.L-1, 21.37 ± 0.77 g.L-1, 0.94 ± 0.05 g.L-1, respectively. After simulated in vitro digestion, the inulin concentration was partially preserved with 20.11 ± 0.21 maltose equivalent (μg.mL-1). The fermented and pre-digested oat beverage (with 7.71 ± 0.44 log CFU.mL-1) was fed into TIM-2, which was previously inoculated with feces from healthy adults. The analysis identified nine bacterial taxa that were significantly modulated compared to the standard ileal effluent medium (SIEM) control. An increase in relative abundance of Lactobacillus and Catenibacterium, and reduction in Citrobacter, Escherichia-Shigella, and Klebsiella was observed. In addition, the cumulative means of short-chain fatty acids (SCFAs) increased, especially for acetate and butyrate. These findings suggest that the developed oat beverage can positively influence the gut microbiota and its activity, highlighting possible health benefits.

The significant depigmentation of brown eggshells occurs in the in the late-phase laying hens, which directly affects consumer acceptance. However, the biological mechanism of eggshell depigmentation based on uterine metabolism has not been elucidated. In this study, a total of 4 group were as follows: 1) 65-week-old laying hens with normal color; 2) 65-week-old laying hens with light color; 3) 80-week-old laying hens with normal color; 4) 80-week-old laying hens with light color. Variations in the pigment contents, uterine antioxidant capacity, uterine microbiota, and uterine metabolomics were examined in current study. Results showed that significantly decreased L* values and increased a* and b* values were observed in the depigmentation group (P < 0.05). The protoporphyrin IX content of the uterus with eggshell depigmentation was significantly decreased in 65-week-old laying hens (P < 0.05). Uterine MDA content was significantly increased in the depigmentation groups at 65 and 80 weeks of age, accompanied by reduced SOD and increased IgA levels (P > 0.05). The abundance of Proteobacteria and Campilobacterota was markedly reduced in the uterus with eggshell depigmentation, whereas Firmicutes was elevated at 65 weeks of age (P < 0.05). Further, Psychrobacte as biomarkers can accurately distinguish between normal color and depigmentation in eggshells (AUC = 0.91). A total of 51 differential metabolites were significantly enriched in the down-regulated sphingolipid metabolism, linoleic acid metabolism, citrate cycle, oxidative phosphorylation, PPAR signaling pathway, FoxO signaling pathway, and apoptosis at 65 weeks of age (P < 0.05). Meanwhile, there were 82 differential metabolites were significantly up-regulated at 80 weeks of age, which mainly enriched in up-regulated linoleic acid metabolism, purine metabolism, and pentose phosphate pathway (P < 0.05). These findings elucidate the specific metabolic mechanisms responsible for eggshell depigmentation in 65- and 80-week-old laying hens, contributing to the improvement of eggshell depigmentation by the precise nutritional modulation in the late-phase laying hens.

Several previous observational studies have shown that abnormal sphingomyelin metabolism may be implicated in the pathogenesis of Alzheimer's disease. To determine the causal relationship between sphingolipid abundance and gut microbiota abundance at the genetic level, we conducted a Mendelian randomization (MR) investigation.

We first used the TwoSampleMR and MRPRESSO packages for conducting two-sample MR studies. Second, we utilized random effect inverse variance weighting (IVW) as the principal method of analysis and used MR‒Egger, the weighted median, the simple mode and the weighted mode as supplementary methods. Finally, we performed tests for heterogeneity and horizontal pleiotropy. These analyses were also conducted to evaluate the impact of individual SNPs on the outcomes of our analysis. A Bonferroni-corrected threshold of p = 2.4e-4(0.05/211) was considered significant, and p values less than 0·05 were considered to be suggestive of an association.

The results showed that sphingolipid levels were suggestively associated with the abundance of 6 gut microbiota taxa. Specifically, two taxa were positively correlated with sphingolipid levels, including the family Alcaligenaceae (p = 0.006, OR 95% CI = 1.109 [1.030-1.194]) and the species Ruminococcus callidus (p = 0.034, OR 95% CI = 1.217 [1.015-1.460]). In contrast, negative correlations were observed with the abundances of 4 gut microbiota taxa, including the genus Flavonifractor (p = 0.026, OR 95% CI = 0.804 [0.663-0.974]), the genus Streptococcus (p = 0.014, OR 95% CI = 0.909 [0.842-0.981]), the species Bacteroides caccae (p = 0.037, OR 95% CI = 0.870 [0.763-0.992]), and the species Haemophilus parainfluenzae (p = 0.006, beta 95% CI = -0.269 [-0.462, -0.076]). The results presented a normal distribution, with no anomalous values, heterogeneity, or horizontal pleiotropic effects detected.

This two-sample MR study revealed a potential causal relationship between sphingomyelin levels and gut microbiota abundance.

Precision health is a person-centered approach to health and well-being that is operationalized through evaluating omics-level profiles and their associations with the exposome. A precision health approach addresses the challenge that "one size does not fit all" in the management of an individual's health.

The purpose of this white paper is to introduce a Precision Health Model and its application in research and clinical care.

An expert panel reviewed and synthesized the extant literature related to precision health, the current state of omics' science, and common exposome factors that influence the health/illness continuum. A case study provides the framework for the application of the Precision Health Model.

Precision health and key domains are defined and serve as the platform for the development of the Precision Health Model.

Application of the Precision Health Model will provide inclusive, equitable, person-centered research and clinical care.

Primary Sjögren's syndrome (pSS) is a complex autoimmune disease characterized by diverse clinical manifestations. While xerophthalmia and xerostomia are hallmark symptoms, the disease often involves multiple organ systems, including the kidneys, lungs, nervous system, and gastrointestinal tract, leading to systemic morbidity in severe cases. Despite extensive research, the precise pathogenesis of pSS remains unclear, likely involving infectious, hormonal, and genetic factors. Emerging evidence highlights the microbiome as a key contributor to autoimmune diseases, including pSS. Dysbiosis in the oral, ocular, gut, and genital microbiomes plays a critical role in disease onset, progression, and variability. This review summarizes current findings on microbiome alterations in pSS, emphasizing their role in pathogenesis and clinical features, and explores microbiome-targeted therapies. Understanding the role of the microbiome in pSS pathophysiology could advance disease management and inspire targeted therapeutic strategies.

Human activities have greatly influenced global temperatures, leading to climate change and global warming. This narrative review aims to explore the relationship between climate change and the immune system, focusing on how environmental stressors can affect immune regulation, leading to both hyperactivity and suppression.

A comprehensive search was conducted in PubMed and Google Scholar for peer-reviewed studies published up to June 2024. The search terms included "climate change," "human health," "infection," "immunity," and "disease." Inclusion criteria were based on relevance, originality, and accessibility.

Exposure to elevated temperatures can significantly impair immune system cells, leading to an overproduction of signaling molecules that promote inflammation. Temperature fluctuations have been shown to influence various aspects of the adaptive immune response, including immune cell mobilization, antigen processing and presentation, lymphocyte trafficking and activation, and the functionality of B and T cells. Notably, some research suggests that heat stress negatively impacts B lymphocyte differentiation, replication, and proportion, resulting in decreased immunoglobulin and cytokine production, and contributing to immunosuppression. Additionally, climate change-related exposures can compromise epithelial barriers in the skin, lungs, and gut, leading to microbial dysbiosis, and immune dysregulation. Furthermore, environmental factors such as temperature variations, humidity, and air pollutant levels may exacerbate the prevalence of infectious diseases, including measles and HIV, with varying impacts on acute, chronic, and latent infections, further contributing to immune variability.

Climate change, particularly increased temperatures, significantly impacts immune system function, leading to both heightened inflammatory responses, and immunosuppression. Future research should focus on developing comprehensive and sustainable management strategies to enhance health resilience in the face of ongoing climatic changes.

Wound infections are still an interdisciplinary and interprofessional challenge, because of numerous complications, particularly in people with chronic wounds. There are many different concepts and approaches in this field today. Therefore, WundDACH, the umbrella organization of the German-speaking wound healing societies, wrote a position paper on this important topic. An interdisciplinary and interprofessional group of experts from German-speaking countries developed definitions and procedures for nomenclature, diagnosis and treatment of wound infections in people with chronic wounds in a modified Delphi process. The importance of correctly diagnosing wound infections is emphasized so that adequate treatment can be carried out as early and specifically as possible. For a differentiated assessment, a simplified continuum of wound infection with contamination, colonization, local and systemic infection and the corresponding therapeutic consequences was described. Most bacteria in wounds can be removed by repeated wound-irrigation and debridement. Local wound infections are diagnosed based on clinical signs of infection and TILI score. Treatment is then usually exclusively local, for example with modern antiseptics such as polyhexanide. Systemic antibiotics should mostly be considered when signs of systemic infections appear. The indication for antimicrobial wound therapy should be critically reviewed after 10-14 days at the latest.

Previous studies found that children with siblings, farm residence, and other proxies of greater microbial contacts had lower rates of hyper-responsive immune disorders. Yet, scientific debate persists regarding whether the human immune system is educated in early life primarily as a function of pathogenic or benign microbial exposures, or both. Furthermore, pregnancy relies on women's intrinsic immunosuppressive function, yet it remained unknown how immunoregulation in pregnant women relates to early-life microbial exposures. Here, we conduct a preliminary examination of whether childhood microbial exposures prime women's pregnancy-related immunoregulatory capacity.

We administered retrospective questionnaires to estimate 55 pregnant women's early-life exposure to pathogenic (e.g., illness) and benign (e.g., pets; rural residence) microbes. Tolerogenic regulatory T-cells (Tregs) and Treg subtypes were measured by flow cytometry from peripheral blood.

Results show that proxies for both pathogenic and benign exposures were positively associated with Treg concentrations.

These findings offer insights that may help elucidate the relative contributions of early-life pathogenic ("hygiene hypothesis") and benign ("old friends hypothesis") microbial exposures toward the expansion of the Treg compartment. Human evolutionary history is characterized by changing microbial exposures as human residency patterns, living environments, and subsistence strategies changed. In this context, our findings suggest the possibility of less gestational pathology in human evolutionary past conditions typified by richer diversity of microbial exposure.

Microbial communities inhabiting various body sites play critical roles in the initiation, progression, and treatment of cancer. The gut microbiota, a highly diverse microbial ecosystem, interacts with immune cells to modulate inflammation and immune surveillance, influencing cancer risk and therapeutic outcomes. Local tissue microbiota may impact the transition from premalignant states to malignancy. Characterization of the intratumoral microbiota increasingly reveals distinct microbiomes that may influence tumor growth, immune responses, and treatment efficacy. Various bacteria species have been reported to modulate cancer therapies through mechanisms such as altering drug metabolism and shaping the tumor microenvironment (TME). For instance, gut or intratumoral bacterial enzymatic activity can convert prodrugs into active forms, enhancing therapeutic effects or, conversely, inactivating small-molecule chemotherapeutics. Specific bacterial species have also been linked to improved responses to immunotherapy, underscoring the microbiome's role in treatment outcomes. Furthermore, unique microbial signatures in cancer patients, compared with healthy individuals, demonstrate the diagnostic potential of microbiota. Beyond the gut, tumor-associated and local microbiomes also affect therapy by influencing inflammation, tumor progression, and drug resistance. This review explores the multifaceted relationships between microbiomes and cancer, focusing on their roles in modulating the TME, immune activation, and treatment efficacy. The diagnostic and therapeutic potential of bacterial members of microbiota represents a promising avenue for advancing precision oncology and improving patient outcomes. By leveraging microbial biomarkers and interventions, new strategies can be developed to optimize cancer diagnosis and treatment.

This study investigated the relationship between risk factors for breast cancer (BC) and the microbiome by comparing the microbiomes of BC patients with fatty liver disease to those with a normal liver. Bacterial extracellular vesicles were collected from each blood sample, and next-generation sequencing was performed. The analysis identified specific microbiome profiles shared among groups with hyperglycaemia, hyperlipidaemia, and high body mass index (BMI), which were then compared with functional biomarkers. In particular, the genus Faecalibacterium was a specific bacterium found in the groups with high concentrations of low-density lipoprotein cholesterol, high BMI, and fatty liver disease. Therefore, when the prognosis of patients with BC was analysed based on Faecalibacterium presence, it was confirmed that patients' prognoses tended to deteriorate. In this study, BC risk factors, such as hyperglycaemia, hyperlipidaemia, fatty liver, and high BMI, were interconnected through the microbiome. This provides insights into how the risk factors for BC are linked and their impact on the microbiome and human health.

Bacterial disease alters the infection court creating new niches. The apoplast is an oasis from the hardships of the leaf surface and is generally inaccessible to nonpathogenic members of the phyllosphere bacterial community. Previously, we demonstrated that Salmonella enterica serovar Typhimurium (S. Typhimurium) immigrants to the leaf surface can both enter the apoplast and replicate due to conditions created by an established Xanthomonas hortorum pv. gardneri (Xhg) infection in tomato. Here, we have expanded our investigation of how infection changes the host by examining the effects of another water-soaking pathogen, Pseudomonas syringae pv. tomato (Pst), on immigrating bacteria. We discovered that, despite causing macroscopically similar symptoms as Xhg, Pst infection disrupts S. Typhimurium colonization of the apoplast. To determine if these effects were broadly applicable to phyllosphere bacteria, we examined the fates of immigrant Xhg and Pst arriving on an infected leaf. We found that this effect is not specific to S. Typhimurium, but that immigrating Xhg or Pst also struggled to fully join the infecting Pst population established in the apoplast. To identify the mechanisms underlying these results, we quantified macroscopic infection symptoms, examined stomata as a pinch point of bacterial entry, and characterized aspects of interbacterial competition. While it may be considered common knowledge that hosts are fundamentally altered following infection, the mechanisms that drive these changes remain poorly understood. Here, we investigated these pathogens to reach a deeper understanding of how infection alters a host from a rarely accessible, inhabitable environment to an obtainable, habitable niche.

The microbiome, comprising the diverse microbial communities inhabiting the human body, has emerged as a critical factor in regulating immune function and inflammation. The relationship between the microbiome and uveitis represents a promising frontier in ophthalmological research, with the microbiome increasingly implicated in disease onset and progression. Research has predominantly focused on the gut microbiome, with animal studies providing evidence that dysbiosis is a key factor in autoimmunity. As the understanding of the microbiome increases, so does the potential for developing innovative treatments that leverage the microbiome's impact on immune and inflammatory processes. Future research will be crucial for deciphering the complexities of the interaction between the microbiome and immune system and for creating effective microbiome-based therapies for those with uveitis. Incorporating microbiome research into clinical practice could transform how uveitis is managed, leading to better and more individualized approaches for management. This review discusses the current understanding of the microbiome-uveitis axis, the promise of microbiome-based diagnostics and therapeutics, and the critical need for large-scale, longitudinal studies. Unlocking the potential of microbiome-targeted approaches may revolutionize the management of uveitis and other inflammatory diseases.

The last decennia have witnessed spectacular advances in our knowledge about the influence of the gut microbiome on the development of a wide swathe of diseases that extend beyond the digestive tract, including skin diseases like psoriasis, atopic dermatitis, acne vulgaris, rosacea, alopecia areata, and hidradenitis suppurativa. The novel concept of the gut-skin axis delves into how skin diseases and the microbiome interact through inflammatory mediators, metabolites, and the intestinal barrier. Elucidating the effects of the gut microbiome on skin health could provide new opportunities for developing innovative treatments for dermatological diseases. Psoriasis is a complex disease with multiple factors contributing to its development, such as diet, lifestyle, genetic predisposition, and the microbiome. This paper has a dual purpose. First, we outline the current knowledge on the unique gut microbiota patterns implicated in the pathogenesis of psoriasis. Second, and of equal importance, we briefly discuss the reciprocal impact of psoriasis treatment and gut microbiome. In addition, this review explores potential therapeutic targets based on microbial interventions, which hold promise for providing new treatment options for psoriasis.

Irritable bowel syndrome (IBS) is a prevalent gastrointestinal disorder, affecting 3-5% of the global population and significantly impacting patients' quality of life and healthcare resources. Alongside physical symptoms such as abdominal pain and altered bowel habits, many individuals experience psychological comorbidities, including anxiety and depression. Recent research has highlighted the critical role of the gut microbiota in IBS, with dysbiosis, characterized by an imbalance in microbial diversity, frequently observed in patients. The gut-brain axis, a bidirectional communication network between the gut and central nervous system, plays a central role in the development of IBS symptoms. Although interventions such as probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) have demonstrated potential in modulating the gut microbiota and alleviating symptoms, their efficacy remains an area of ongoing investigation. This review examines the interactions between the gut microbiota, immune system, and brain, emphasizing the need for personalized therapeutic strategies. Future research should aim to identify reliable microbiota-based biomarkers for IBS and refine microbiome-targeted therapies to enhance patient outcomes.

This study aims to evaluate differences in gut microbiota structures between infertile women undergoing frozen embryo transfer (FET) with gestational diabetes mellitus (GDM) and healthy controls (HCs), and to identify potential markers. We comprehensively enrolled 193 infertile women undergoing FET (discovery cohort: 38 HCs and 31 GDM; validation cohort: 85 HCs and 39 GDM). Gut microbial profiles of the discovery cohort were investigated during the pre-pregnancy (Pre), first trimester (T1), and second trimester (T2). The microbial community in the HCs group remained relatively stable throughout the pregnancy, while the microbial structure alteration occurred in the GDM group during T2. A model based on ten bacteria and ten metabolites simultaneously was used to predict the risk of GDM developing in the pre-pregnancy state with the ROC value of 0.712. Algorithms on the basis of marker species and biochemical parameters can be used as effective tools for GDM risk evaluation before pregnancy.

Bacteria constitute the most abundant life form on earth, of which the majority exist in a protective biofilm state. Since the 1980s, we have learned much about the role of biofilm in human chronic infections, with associated global healthcare costs recently estimated at ~$386 billion. Chronic wound infection is a prominent biofilm-induced condition that is characterised by persistent inflammation and associated host tissue destruction, and clinical signs that are distinct from signs of acute wound infection. Biofilm also enables greater tolerance to antimicrobial agents in chronic wound infections compared with acute wound infections. Given the difficulty in eliminating wound biofilm, a multi-targeted strategy (namely biofilm-based wound care) involving debridement and antimicrobial therapies were introduced and have been practiced since the early 2000s. More recently, acknowledgement of the speed at which biofilm can develop and hence quickly interfere with wound healing has highlighted the need for an early anti-biofilm strategy to combat biofilm before it takes control and prevents wound healing. This strategy, referred to as wound hygiene, involves multiple tools in combination (debridement, cleansing, and antimicrobial dressings) to maximise success in biofilm removal and encourage wound healing. This review is intended to highlight the issues and challenges associated with biofilm-induced chronic infections, and specifically address the challenges in chronic wound management, and tools required to combat biofilm and encourage wound healing.

Microbiomes provide key contributions to health and potentially important therapeutic targets. Conceived nearly 30 years ago, the prebiotic concept posits that targeted modulation of host microbial communities through the provision of selectively utilized growth substrates provides an effective approach to improving health. Although the basic tenets of this concept remain the same, it is timely to address certain challenges pertaining to prebiotics, including establishing that prebiotic-induced microbiota modulation causes the health outcome, determining which members within a complex microbial community directly utilize specific substrates in vivo and when those microbial effects sufficiently satisfy selectivity requirements, and clarification of the scientific principles on which the term 'prebiotic' is predicated to inspire proper use. In this Expert Recommendation, we provide a framework for the classification of compounds as prebiotics. We discuss ecological principles by which substrates modulate microbiomes and methodologies useful for characterizing such changes. We then propose statistical approaches that can be used to establish causal links between selective effects on the microbiome and health effects on the host, which can help address existing challenges. We use this information to provide the minimum criteria needed to classify compounds as prebiotics. Furthermore, communications to consumers and regulatory approaches to prebiotics worldwide are discussed.

To perform a scientometric analysis of scientific literature related to microbiota and periodontitis.

A search strategy was applied on 21 July 2024, identifying 1,069 papers from 408 different sources. However, nine articles could not be exported to SciVal due to incomplete metadata. The documents, including 722 articles, 282 reviews, 44 book chapters, among others, showed an annual growth rate of 7.53%. Bibliometrix and SciVal were used for data extraction and analysis.

A total of 1,069 papers from 408 different sources, published between 2019 and 2024, were identified. The most frequent terms in the research were "periodontitis", "oral microbiome", "microbiome", "periodontal disease", and "dysbiosis". According to Lotka's Law, most authors in the field contributed a small number of papers. The most cited journals in this field were "Frontiers in Cellular and Infection Microbiology", "Journal of Oral Microbiology", and "Periodontology 2000". Analysis of the thematic evolution shows an increasing intersection of topics in recent research, reflecting the multifaceted nature of periodontitis and its interaction with a variety of other health factors.

Research on periodontitis and microbiota is multifaceted, interacts with a variety of health factors, and shows a growing intersection of topics in recent research.

This study presents a detailed review of the literature on gut microbiota and periodontitis, notes on current developments, and gives hints regarding still emerging themes. Its findings may serve to continue with future guidelines or research and to understand the relationship of gut microbiota with periodontitis. How to cite this article: Mayta-Tovalino F, Espinoza-Carhuancho F, Huaman-De la Cruz M, et al. Scientometric Analysis of Research on Oral and Gut Microbiota and Periodontitis: Collaborative Networks, Emerging Patterns, Thematic Evolution. J Contemp Dent Pract 2025;26(1):86-92.

Objective: Biotics are increasingly being used in the treatment of irritable bowel syndrome (IBS). This study aimed to assess the efficacy and safety of a mixture of microencapsulated sodium butyrate, probiotics (Lactocaseibacillus rhamnosus DSM 26357, Lactobacillus acidophilus DSM 32418, Bifidobacterium longum DSM 32946, Bifidobacterium bifidum DSM 32403, and Bifidobacterium lactis DSM 32269), and short-chain fructooligosaccharides (scFOSs) in IBS patients. Methods: This was a randomized, double-blind, placebo-controlled trial involving 120 adult participants with IBS. The primary outcome of the 12-week intervention was the improvement in IBS symptoms and quality of life (QOL), assessed with the use of IBS-Adequate Relief (IBS-AR), IBS-Global Improvement Scale (IBS-GIS), IBS-Symptom Severity Score (IBS-SSS), and IBS-QOL. Secondary outcomes were the number and type of stools (assessed via the Bristol Stool Form scale), patient-recorded symptoms, anthropometric parameters, and levels of selected inflammatory cytokines. Results: As early as at 4 weeks, there was a higher percentage of patients in the biotic group reporting adequate relief of symptoms (based on IBS-AR) than in the placebo group (64.7% vs. 42.0%, respectively, p = 0.023). At 12 weeks, fewer patients in the biotic group reported a 'worsening of symptoms' (based on IBS-GIS) than in the placebo group (5.9% vs. 16.0% respectively, p = 0.015). There were no significant differences between groups in IBS-QOL or IBS-SSS or any of the secondary outcome measures except the patient-recorded 'urgency to defecate' (p = 0.015) at week 12, which was significantly lower in the biotic group. The intervention was safe and well tolerated. Conclusions: A biotic mixture consisting of microencapsulated butyrate, probiotics, and small amounts of scFOSs is safe and effective in improving gastrointestinal symptoms in patients with IBS.

Periodontal disease is characterized by bacterial toxins within the oral biofilm surrounding the teeth, leading to gingivitis and the gradual dissolution of the alveolar bone, which supports the teeth. Notably, symptoms in the early stages of the disease are often absent. Similarly, dental caries occurs when oral bacteria metabolize dietary sugars, producing acids that dissolve tooth enamel and dentin. These bacteria are commonly present in the oral cavity of most individuals. Metabolomics, a relatively recent addition to the "omics" research landscape, involves the comprehensive analysis of metabolites in vivo to elucidate pathological mechanisms and accelerate drug discovery. Meanwhile, the term "microbiome" refers to the collection of microorganisms within a specific environmental niche or their collective genomes. The human microbiome plays a critical role in health and disease, influencing a wide array of physiological and pathological processes. Recent advances in microbiome research have identified numerous bacteria implicated in dental caries and periodontal disease. Additionally, studies have uncovered various pathogenic factors associated with these microorganisms. This review focuses on recent findings in metabolomics and the microbiome, specifically targeting oral bacteria linked to dental caries and periodontal disease. We acknowledge the limitation of relying exclusively on the MEDLINE database via PubMed, while excluding other sources such as gray literature, conference proceedings, and clinical practice guidelines.

Historically, the multiple uses of cannabis as a medicine, food, and for recreational purposes as a psychoactive drug span several centuries. The various components of the plant (i.e., seeds, roots, leaves and flowers) have been utilized to alleviate symptoms of inflammation and pain (e.g., osteoarthritis, rheumatoid arthritis), mood disorders such as anxiety, and intestinal problems such as nausea, vomiting, abdominal pain and diarrhea. It has been established that the intestinal microbiota progresses neurological, endocrine, and immunological network effects through the gut-microbiota-brain axis, serving as a bilateral communication pathway between the central and enteric nervous systems. An expanding body of clinical evidence emphasizes that the endocannabinoid system has a fundamental connection in regulating immune responses. This is exemplified by its pivotal role in intestinal metabolic and immunity equilibrium and intestinal barrier integrity. This neuromodulator system responds to internal and external environmental signals while also serving as a homeostatic effector system, participating in a reciprocal association with the intestinal microbiota. We advance an exogenous cannabinoid-intestinal microbiota-endocannabinoid system axis potentiated by the intestinal microbiome and medicinal cannabinoids supporting the mechanism of action of the endocannabinoid system. An integrative medicine model of patient care is advanced that may provide patients with beneficial health outcomes when prescribed medicinal cannabis.

The complex symbiotic relationship between inflammation, the gut microbiota, and the central nervous system (CNS) has become a pivotal focus of contemporary biomedical research. Inflammation, as a physiological defense mechanism, plays a dual role as both a protective and pathological factor, and is intricately associated with gut microbiota homeostasis, often termed the "second brain." The gutbrain axis (GBA) exemplifies this multifaceted interaction, where gut health exerts significantly regulatory effects on CNS functions. Antibacterial therapies represent both promising and challenging strategies for modulating inflammation and gut microbiota composition to confer CNS benefits. However, while such therapies may exert positive modulatory effects on the gut microbiota, they also carry the potential to disrupt microbial equilibrium, potentially exacerbating neurological dysfunction. Recent advances have provided critical insights into the therapeutic implications of antibacterial interventions; nevertheless, the application of these therapies in the context of CNS health warrants a judicious and evidence-based approach. As research progresses, deeper investigation into the microbial-neural interface is essential to fully realize the potential of therapies targeting inflammation and the gut microbiota for CNS health. Future efforts should focus on refining antibacterial interventions to modulate the gut microbiota while minimizing disruption to microbial balance, thereby reducing risks and enhancing efficacy in CNS-related conditions. In conclusion, despite challenges, a more comprehensive understanding of the GBA, along with precise modulation through targeted antibacterial therapies, offers significant promise for advancing CNS disorder treatment. Continued research in this area will lead to innovative interventions and improved patient outcomes.

Benzalkonium chlorides (BACs) are commonly used disinfectants in a variety of consumer and food-processing settings, and the COVID-19 pandemic has led to increased usage of BACs. The prevalence of BACs raises the concern that BAC exposure could disrupt the gastrointestinal microbiota, thus interfering with the beneficial functions of the microbes. We hypothesize that BAC exposure can alter the gut microbiome diversity and composition, which will disrupt bile acid (BA) homeostasis along the gut-liver axis. In this study, male and female mice were exposed orally to d7-C12- and d7-C16-BACs at 120 µg/g/d for 1 wk. UPLC-MS/MS analysis of liver, blood, and fecal samples of BAC-treated mice demonstrated the absorption and metabolism of BACs. Both parent BACs and their metabolites were detected in all exposed samples. Additionally, 16S rRNA sequencing was carried out on the bacterial DNA isolated from the cecum intestinal content. For female mice, and to a lesser extent in males, we found that treatment with either d7-C12- or d7-C16-BAC led to decreased alpha diversity and differential composition of gut bacteria with notably decreased actinobacteria phylum. Lastly, through a targeted BA quantitation analysis, we observed decreases in secondary BAs in BAC-treated mice, which was more pronounced in the female mice. This finding is supported by decreases in bacteria known to metabolize primary BAs into secondary BAs, such as the families of Ruminococcaceae and Lachnospiraceae. Together, these data signify the potential impact of BACs on human health through disturbance of the gut microbiome and gut-liver interactions.

Depletion of Lactobacillus species and an overgrowth of anaerobes in the vaginal tract bacterial vaginosis (BV)], is associated with non-optimal reproductive health outcomes, and increased susceptibility to sexually transmitted infections (STIs). BV is currently treated with antibiotics, although these provide suboptimal cure levels and high recurrence rates. Vaginal microbiota transplantation (VMT), the transfer of vaginal fluid from healthy donors with an optimal vaginal microbiota to a recipient with BV, has been proposed as an alternative treatment strategy.

Here, we investigated knowledge and perceptions of blood donors to the concept of an optimal vaginal microbiome and VMT via the Western Cape Blood Service (WCBS) clinics in Cape Town, South Africa, by a self-administered questionnaire.

Analysis of responses from 106 eligible women showed that 86% (91/106) would consider donating samples. Responses significantly associated with willingness to donate vaginal samples included: (1) belief that helping others outweighs the inconvenience of donating vaginal sample (p = 1.093e-05) and (2) prior knowledge of the concept of a healthy vaginal microbiome (p = 0.001). Most potential donors (59/91; 65%) were willing to receive a VMT themselves if needed. Participants who were unwilling to donate vaginal samples (15/106; 14%) indicated that vaginal sample collection would be unpleasant and/or embarrassing. The benefits of a collaboration with WCBS for this project include the naturally altruistic nature of blood donors, the constant in-flow of donors to WCBS clinics, and the infrastructure and logistical aspects in place. Data from this observational study highlight factors affecting the willingness of blood donors to become vaginal sample donors.

Endometriosis is a chronic, complex, systemic inflammatory condition that impacts approximately 190 million girls and women worldwide, significantly impacting their quality of life. The effective management of endometriosis requires a multi-disciplinary and holistic approach, one that includes surgical and medical management, such as a laparoscopy and a chronic medical management plan, as well as dietary, nutritional, and lifestyle adjunct interventions, such as pelvic pain physiotherapy and acupuncture. There is growing evidence to support the role of dietary and nutritional interventions in the adjunct management of endometriosis-related pain and gastrointestinal symptoms. However, the implementation of these interventions is often not regulated, as patients with endometriosis often adopt self-management strategies. Diet and nutrition can modulate key players integral to the pathophysiology of endometriosis, such as, but not limited to, inflammation, estrogen, and the microbiome. However, it is unclear as to whether diet plays a role in the prevention or the onset of endometriosis. In this review, we discuss three key players in the pathogenesis of endometriosis-inflammation, estrogen, and the microbiome-and we summarize how diet and nutrition can influence their mechanisms, and consequently, the progression and manifestation of endometriosis. There is a major need for evidence-based, non-invasive adjunct management of this debilitating disease, and diet and nutritional interventions may be suitable.

Beside the respiratory tract, the skin and the gut represent the first defensive lines of our body against the external insults displaying many important biochemical features able to maintain the epithelial barrier integrity and to regulate the tissue immune responses. The human microbiome is essential in maintaining the tissue homeostasis and its dysregulation may lead to tissue conditions including inflammatory pathologies. Among all external insults, air pollutants have been shown to cause oxidative stress damage within the target tissues via an OxInflammatory response. Dysregulation of the gut microbiome (dysbiosis) by outdoor stressors, including air pollutants, may promote the exacerbation of the skin tissue damage via the interplay between the gut-skin axis. The intent of this review is to highlight the ability of exogenous stressors to modulate the human gut-skin axis via a redox regulated mechanism affecting the microbiome and therefore contributing to the development and aggravation of gut and skin conditions.

Glaucoma is the primary cause of irreversible blindness globally. Different glaucoma subtypes are identified by their underlying mechanisms, and treatment options differ by its pathogenesis. Current management includes topical medications to lower intraocular pressure and surgical procedures like trabeculoplasty and glaucoma drainage implants. Fecal microbiota transplantation (FMT) is an almost effective and safe treatment option for recurrent Clostridium difficile infection. The relationship between bacterial populations, metabolites, and inflammatory pathways in retinal diseases indicates possible therapeutic strategies. Thus, incorporating host microbiota-based therapies could offer an additional treatment option for glaucoma patients. Here, we propose that combining FMT with standard glaucoma treatments may benefit those affected by this condition. Also, the potential safety, efficacy, cost-effectiveness and clinical applications are discussed.

The impacts and toxicological mechanisms of microplastics (MPs) or heavy metals on aquatic ecosystems have been the subject of extensive research and initial understanding. However, the combined toxicity of co-pollutants on organisms and cumulative toxic effects along the food chain are still underexplored. In this study, the ciliate protozoan Paramecium caudatum and zebrafish Danio rerio were used to represent the microbial loop and the higher trophic level, respectively, to illustrate the progressive exposure of MPs and cadmium (Cd2+). The findings indicate that MPs (ca. 1 ×105 items/L) containing with Cd2+ (below 0.1 µg/L) could permeate the bodies of zebrafish through trophic levels after primary ingestion by ciliates. This could cause adverse effects on zebrafish, including alterations in bioindicators (total sugar, triglycerides, lactate, and glycogen) associated with metabolism, delayed hepatic development, disruption of intestinal microbiota, DNA damage, inflammatory responses, and abnormal cellular apoptosis. In addition, the potential risks associated with the transfer of composite pollutants through the microbial loop into traditional food chain were examined, offering novel insights on the evaluation of the ecological risks associated with MPs. As observed, understanding the bioaccumulation and toxic effects of combined pollutants in zebrafish holds crucial implications for food safety and human health.

Ocular surface inflammatory disorders, such as dry eye, are becoming increasingly prevalent. Developing new treatment strategies targeting harmful bacteria could provide significant therapeutic benefits. The purpose of this study was to characterize the common ocular pathogen Staphylococcus aureus and the rarer endophthalmitis-associated species Enterococcus faecalis isolated from the ocular surface of dry eye disease patients in Norway. Together the 7 isolates (5 S. aureus and 2 E. faecalis) comprise the complete set of members of each species isolated in our previous study of the ocular microbiome of 61 dry eye sufferers. We aimed to investigate the pathogenic potential of these isolates in relation to ocular surface health. To this end, we used whole genome sequencing, multiplex PCR directed at virulence genes and antibiotic susceptibility tests encompassing clinically relevant agents. The E. faecalis isolates showed resistance to only gentamicin. S. aureus isolates displayed susceptibility to most of the tested antibiotics, except for two isolates which showed resistance to trimethoprim/sulfamethoxazole and three isolates which were resistant to ampicillin. Susceptibilities included sensitivity to several first-line antibiotics for treatment of ocular infections by these species. Thus, treatment options would be available if required. However, spontaneous resistance development to gentamicin and rifampicin occurred in some S. aureus which could be a cause for concern. Whole genome sequencing of the isolates showed genome sizes ranging from 2.74 to 2.83 Mbp for S. aureus and 2.86 Mbp for E. faecalis, which is typical for these species. Multilocus sequence typing and phylogenetic comparisons with previously published genomes, did not suggest the presence of eye-specific clusters for either species. Genomic analysis indicated a high probability of pathogenicity among all isolates included in the study. Resistome analysis revealed the presence of the beta-lactamase blaZ gene in all S. aureus isolates and the dfrG gene in two of them; while E. faecalis isolates carried the lsa(A) gene which confers intrinsic resistance to lincosamides and streptogramin A in this species. Screening for virulence factors revealed the presence of various pathogenicity associated genes in both S. aureus and E. faecalis isolates. These included genes coding for toxin production and factors associated with evading the host immune system. Some of the identified genes (tst, hylA & hylB) are suggested to be linked to the pathophysiology of dry eye disease. Lastly, the presence of specific S. aureus virulence genes was confirmed through multiplex PCR analysis.

Gastric cancer (GC) is one of the most common cancers worldwide. Most patients are diagnosed at the progressive stage of GC, and progress in the development of effective anti-GC drugs has been insufficient. The tumor microenvironment (TME) regulates various functions of tumor cells, and interactions between the cellular and molecular components of the TME-e.g., inflammatory cells, fibroblasts, vasculature cells, and innate and adaptive immune cells-promote the aggressiveness of cancer cells and dissemination to distant organs. This review summarizes the roles of various TME cells and molecules in regulating the malignant progression and metastasis of GC. We also address the important roles of signaling pathways in mediating the interaction between cancer cells and the different components of the GC TME. Finally, we discuss the implications of these molecular mechanisms for developing novel and effective therapies targeting molecular and cellular components of the GC TME to control the malignant progression of GC.

The microbiome-gut-brain axis is altered by environmental stressors such as heat, diet, and pollutants as well as microbes in the air, water, and soil. These stressors might alter the host's microbiome and symbiotic relationship by modifying the microbial composition or location. Compartmentalized mutualistic microbes promote the beneficial interactions in the host leading to circulating metabolites and hormones such as insulin and leptin that affect inter-organ functions. Inflammation and oxidative stress induced by environmental stressors may alter the composition, distribution, and activities of the microbes in the microbiomes such that the resultant metabolite and hormone changes are no longer beneficial. The microbiome-gut-brain axis and immune adverse changes that may accompany environmental stressors are reviewed for effects on innate and adaptive immune cells, which may make host immunity less responsive to pathogens and more reactive to self-antigens. Cardiovascular and fluid exchanges to organs might adversely alter organ functionality. Organs, especially the brain, need a consistent supply of nutrients and clearance of debris; disruption of these exchanges by stressors, and involvement of gut microbiome are discussed regarding neural dysfunctions with Alzheimer's disease, autistic spectrum disorders, viral infections, and autoimmune diseases. The focus of this review includes the manner in which environmental stressors may disrupt gut microbiota leading to adverse immune and hormonal influences on development of neuropathology related to hyperhomocysteinemia, inflammation, and oxidative stress, and how certain therapeutics may be beneficial. Strategies are explored to lessen detrimental effects of environmental stressors on central and peripheral health navigated toward (1) understanding neurological disorders and (2) promoting environmental and public health and well-being.

The role of gut microbiota in health and disease is being thoroughly examined in various contexts, with a specific focus on the bacterial fraction due to its significant abundance. However, despite their lower abundance, viruses within the gut microbiota are gaining recognition for their crucial role in shaping the structure and function of the intestinal microbiota, with significant effects on the host as a whole, particularly the immune system. Similarly, environmental factors such as stress are key in modulating the host immune system, which in turn influences the composition of the gut virome and neurological functions through the bidirectional communication of the gut-brain axis. In this context, alterations in the host immune system due to stress and/or dysbiosis of the gut virome are critical factors in the development of both infectious and noninfectious diseases. The molecular mechanisms and correlation patterns between microbial species are not yet fully understood. This literature review seeks to explore the interconnected relationship between stress and the gut virome, with a focus on how this interaction is influenced by the host's immune system. We also discuss how disturbances in this finely balanced system can lead to the onset and/or progression of diseases.

The human microbiome is a diverse ecosystem of microorganisms that reside in the body and influence various aspects of health and well-being. Recent advances in sequencing technology have brought to light microbial communities in organs and tissues that were previously considered sterile. The gut microbiota plays an important role in host physiology, including metabolic functions and immune modulation. Disruptions in the balance of the microbiome, known as dysbiosis, have been linked to diseases such as cancer, inflammatory bowel disease and metabolic disorders. In addition, the administration of antibiotics can lead to dysbiosis by disrupting the structure and function of the gut microbial community. Targeting strategies are the key to rebalancing the microbiome and fighting disease, including cancer, through interventions such as probiotics, fecal microbiota transplantation (FMT), and bacteria-based therapies. Future research must focus on understanding the complex interactions between diet, the microbiome and cancer in order to optimize personalized interventions. Multidisciplinary collaborations are essential if we are going to translate microbiome research into clinical practice. This will revolutionize approaches to cancer prevention and treatment.

The importance of the complex interplay between the microbiome and mucosal immunity, particularly within the respiratory tract, has gained significant attention due to its potential implications for the severity and progression of lung diseases. Therefore, this review summarizes the specific interactions through which the respiratory tract-specific microbiome influences mucosal immunity and ultimately impacts respiratory health. Furthermore, we discuss how the microbiome affects mucosal immunity, considering tissue-specific variations, and its capacity in respiratory diseases containing asthma, chronic obstructive pulmonary disease, and lung cancer. Additionally, we investigate the external factors which affect the relationship between respiratory microbiome and mucosal immune responses. By exploring these intricate interactions, this review provides valuable insights into the potential for microbiome-based interventions to modulate mucosal immunity and alleviate the severity of respiratory diseases.

Psoriasis (PS) and inflammatory bowel disease (IBD) are immune-mediated chronic conditions that share pathophysiological processes, including immune system dysfunction, microbiome dysbiosis, and inflammatory pathways. These pathways result in increased turnover of epithelial cells and compromised barrier function. The assessment of the literature suggests that immunopathogenic mechanisms, such as tumor necrosis factor (TNF)-α signaling and IL-23/IL-17 axis dysregulation, are shared by PS and IBD. Clinical characteristics and diagnostic approaches overlap significantly, and advances in biomarker identification benefit both conditions. Current treatments, namely biologics that target TNF-α, IL-17, and IL-23, show promising results in decreasing inflammation and controlling symptoms. Precision medicine approaches are prioritized in prospective therapeutic procedures to tailor pharmaceuticals based on specific biomarkers, perhaps improving outcomes and minimizing side effects. This study thoroughly examines and evaluates the body of research on PS and IBD. Several papers were examined to compile data on clinical features, diagnosis, therapies, pathophysiology, epidemiology, and potential future therapeutic developments. The selection of articles was based on three methodological qualities: relevance and addition to the knowledge of IBD and PS. The retrieved data were combined to provide a coherent summary of the state of the knowledge and to spot new trends. The overview of the latest studies demonstrates that both PS and IBD share pathophysiological foundations and therapeutic approaches. With a spotlight on particular biomarkers, advances in precision medicine provide a promising path toward enhancing therapeutic effectiveness and minimizing side effects.

Bacterial pathogens are responsible for a variety of human diseases, necessitating their prompt detection for effective diagnosis and treatment of infectious diseases. Over recent years, electrochemical methods have gained significant attention owing to their exceptional sensitivity and rapidity. This review outlines the current landscape of electrochemical biosensors employed in clinical diagnostics for the detection of bacterial pathogens. We categorize these biosensors into four types: amperometry, potentiometry, electrochemical impedance spectroscopy, and conductometry, targeting various bacterial components, including toxins, virulence factors, metabolic activity, and events related to bacterial adhesion and invasion. We discuss the merits and challenges associated with electrochemical methods, underscoring their rapid response, high sensitivity, and specificity, while acknowledging the necessity for skilled operators and potential interference from biological and environmental factors. Furthermore, we examine future prospects and potential applications of electrochemical biosensors in clinical diagnostics. While electrochemical biosensors offer a promising avenue for detecting bacterial pathogens, further research in optimizing the robustness and surmounting the challenges hindering their seamless integration into clinical practice is imperative.

The microbiome is a complex ecosystem of microorganisms that inhabit a specific environment. It plays a significant role in human health, from food digestion to immune system strengthening. The "Novel Foods" refer to foods or ingredients that have not been consumed by humans in the European Union before 1997. Currently, there is growing interest in understanding how "Novel Foods" affect the microbiome and human health. The aim of this review was to assess the effects of "Novel Foods" on the human gut microbiome. Research was conducted using scientific databases, focusing on the literature published since 2000, with an emphasis on the past decade. In general, the benefits derived from this type of diet are due to the interaction between polyphenols, oligosaccharides, prebiotics, probiotics, fibre content, and the gut microbiome, which selectively promotes specific microbial species and increases microbial diversity. More research is being conducted on the consumption of novel foods to demonstrate how they affect the microbiome and, thus, human health. Consumption of novel foods with health-promoting properties should be further explored to maintain the diversity and functionality of the gut microbiome as a potential tool to prevent the onset and progression of chronic diseases.

3-indoxyl sulfate (3-IS) results from a hepatic transformation of indole, a tryptophan degradation product produced by commensal gut bacteria. The metabolite has shown promise as a biomarker of dysbiosis and clinical outcomes following hematopoietic stem cell transplant (HSCT) in adults. Nonetheless, there is a paucity of data regarding microbiome health and outcomes in the pediatric HSCT setting. We developed and thoroughly validated an affordable high-performance liquid chromatography/fluorescence detector (HPLC-FLD) method to quantify 3-IS in urine for use in the pediatric setting. Chromatographic separation was achieved on a C18 column (250 × 4.6 mm × 5 μm) with a mobile phase consisting of pH 4.0 acetic acid-triethylamine buffer and acetonitrile (88:12, v/v), eluted isocratically at 1 mL/min. 3-IS fluorescence detection was set at excitation/emission of 280 and 375, respectively. The method was fully validated according to FDA-specified limits including selectivity, linearity (0.10 to 10.00 mg/L, r2 > 0.997), intra- and inter-day accuracy, and precision. 3-IS stability was confirmed after three freeze-thaw cycles, for short- and medium-term on a benchtop and at 4 °C and for long-term up to 60 days at -20 °C. The validated method was used to quantify 3-IS in urine samples from HSCT pediatric patients.

Mold growth on body donations remains an underreported yet serious issue in anatomical teaching. Bacterial and fungal growth pose health risks to lecturers and students, alongside with ethical and aesthetic concerns. However, limited information exists on the presence of bacteria and fungi on body donations and their underlying causes. To investigate the potential impact of airborne germs on body donation contamination, we conducted indoor air measurements before, during, and after our anatomical dissection course, with outdoor measurements serving as a control. Tissue samples from the dissected body donations were collected to assess the germ load, with qualitative and quantitative microbiological analyses. Air samples from the dissection hall contained no fungi, but various fungal species were identified in the adjacent stairways and outdoors which implies that fungal occurrence in the dissection hall air was independent of lecturers' and students' presence. Moreover, our results indicate that adequate ventilation filters can effectively reduce indoor fungal germs during courses, while the bacterial load in room air appears to increase, likely due to the presence of lecturers and students. Additionally, the tissue samples revealed no bacterial or fungal germs which implies that our ethanol-formalin-based embalming solution demonstrates an effective long-term antimicrobial preservation of corpses.

Although the pathogenesis of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), has not been fully elucidated, accumulating researches suggest that intestinal microbiota imbalance contributes to the development of IBD in patients and animal models. RDP58, a peptide-based computer-assisted rational design, has been demonstrated to be effective in protecting against a wide range of autoimmune and inflammatory diseases. However, the underlying mechanism by which RDP58 protects against IBD mediated by intestinal microbiota has yet to be elucidated.

The colitis model was induced by continuously administering 2.5 % (wt/vol) dextran sodium sulfate (DSS) solution for 7 days. The manifestations of colon inflammation were assessed via daily weight changes, colon length, tumor necrosis factor-alpha (TNF-α) level, disease activity index (DAI) score, pathology score, and intestinal barrier permeability. Intestinal microbiota analysis was carried out by 16S-rRNA sequencing. Colonic short chain fatty acids (SCFAs) and regulatory T cells (Tregs) were also detected. To further confirm the protective effect of RDP58 on intestinal microbiota, broad-spectrum antibiotic cocktail (ABX) treatment and fecal microbial transplantation (FMT) experiment were performed.

Oral administration of RDP58 ameliorated DSS-induced mice colitis by altering the diversity and composition of intestinal microbiota. Notably, RDP58 significantly upregulated SCFAs-producing microbiota, thereby promoting the generation of Tregs. ABX and FMT were performed to verify the above mechanism.

RDP58 ameliorated DSS-induced colitis through altering intestinal microbiota and enhancing SCFAs and Tregs production in intestinal microbiota dependent manner, potentially provide a novel therapy for IBD.

Endocrine-disrupting chemicals (EDCs) have become so pervasive in our environment and daily lives that it is impossible to avoid contact with such compounds, including pregnant women seeking to minimize exposures to themselves and their unborn children. Developmental exposure of humans and rodent models to bisphenol A (BPA) and other EDCs is linked to increased anxiogenic behaviors, learning and memory deficits, and decreased socio-sexual behaviors. Prenatal exposure to BPA and other EDCs leads to longstanding and harmful effects on gut microbiota with reductions in beneficial bacteria, i.e., gut dysbiosis, and such microbial changes are linked to host changes in fecal metabolites, including those involved in carbohydrate metabolism and synthesis, and neurobehavioral alterations in adulthood, in particular, social and cognitive deficits. Gut dysbiosis is increasingly being recognized as a key driver of a myriad of diseases, ranging from metabolic, cardiovascular, reproductive, and neurobehavioral disorders via the gut-microbiome-brain axis. Thus, EDCs might induce indirect effects on physical and mental health by acting as microbiome-disrupting chemicals. Findings raise the important question as to whether pregnant women should consume a probiotic supplement to mitigate pernicious effects of EDCs, especially BPA, on themselves and their unborn offspring. Current studies investigating the effects of maternal probiotic supplementation on pregnant women's health and that of their unborn offspring will be reviewed. Data will inform on the potential application of probiotic supplementation to reverse harmful effects of EDCs, especially BPA, in pregnant women unwittingly exposed to these compounds and striving to give their offspring the best start in life.

No organ system better integrates interconnectivity across specialties and disciplines than the microbiome. Scientific focus is shifting from microbes as harbingers of disease toward microbes as symbiotic, balanced, commensal ecologies.

The study intended to discuss and examine the human microbiome, including its development in early life; its impact on various physiological processes that occur throughout the body; and its relationship to dysbiosis; and to investigate microbial mechanisms with clinical applicability across medical specialties.

The study took place at Biocidin Botanicals in Watsonville CA, USA.

Accumulating research upholds the human microbiome as both a predictive biomarker for disease risk and a viable treatment option for modulating the course of illness. Prebiotic and probiotic interventions continue to demonstrate clinical utility, particularly for gastrointestinal, dermatological, inflammatory, metabolic, and mental-health disorders.

Just as germ theory revolutionized infection control in the twentieth century, microbiome systems science stands to transform the conceptualization of health as the balanced coexistence of human and microbial cells in the twenty-first century.

Given the physiological function and anatomical location of the reproductive tract, studying the upper reproductive tract microbiota may be essential for studying male infertility and other male diseases. This study aimed to characterize the microbiota of the upper reproductive tract male rats and investigate whether specific microbial compositions are associated with sperm parameters. 16S rRNA gene sequencing was used to characterize the microbial composition in the testis, epididymis, seminal vesicles, vas deferens and prostate tissues of the rats. The results showed significant enrichment of Methyloperoxococcus spp. in testicular tissues, Jeotgalicoccus spp. in epididymal tissues. Spearman's correlation analysis revealed that the abundance of several bacterial genera in epididymal, testicular, and seminal vesicle gland tissues correlated with several sperm activity parameters. Our findings provide detailed information on characterizing the upper reproductive tract microbiome in male rats, as well as a potentially crucial link between the reproductive system microbiota and sperm quality.