Non-tuberculous mycobacteria (NTM) are emerging pathogens of global concern, particularly in regions with declining tuberculosis rates. This review synthesizes current evidence on the epidemiology, immune pathogenesis, and microbiome interactions underlying NTM infections. The rising incidence of NTM is driven by environmental factors, immunocompromised populations, and advanced diagnostics. Clinically, NTM manifests as pulmonary, lymphatic, skin/soft tissue, or disseminated disease, with Mycobacterium avium complex (MAC) and M. abscessus being predominant pathogens. Host immunity, particularly Th1 responses mediated by IL-12/IFN-γ and TLR2 signaling, is critical for controlling NTM, while dysregulated immunity (e.g., elevated Th2 cytokines, PD-1/IL-10 pathways) exacerbates susceptibility. Emerging research highlights the gut-lung axis as a pivotal mediator of disease, where microbiome dysbiosis-marked by reduced Prevotella and Bifidobacterium-impairs systemic immunity and promotes NTM progression. Short-chain fatty acids (SCFAs) and microbial metabolites like inosine modulate macrophage and T-cell responses, offering therapeutic potential. Studies reveal distinct airway microbiome signatures in NTM patients, characterized by enriched Streptococcus and Prevotella, and reduced diversity linked to worse outcomes. Despite advances, treatment remains challenging due to biofilm formation, antibiotic resistance, and relapse rates. This review underscores the need for microbiome-targeted therapies, personalized medicine, and longitudinal studies to unravel causal relationships between microbial ecology and NTM pathogenesis.

Irritable bowel syndrome (IBS) is one of the most prevalent gastrointestinal (GI) disorders worldwide. Defined as a disorder of gut-brain interaction, its pathophysiology is still not completely clear. Consequently, current treatments primarily target symptoms rather than addressing the cause of the condition. The gut microbiome is increasingly acknowledged as central to IBS pathophysiology and, thus, may have therapeutic potential. Several national treatment guidelines recommend increasing physical activity for IBS management.

This review summarises the evidence about the relationship between physical activity, IBS symptoms, and the gut microbiome, investigating the hypothesis that physical activity's therapeutic effects on IBS may be explained via modulation of the gut microbiome.

This review revealed that routine exercise was associated with a 15%-66% reduction in symptom severity and up to 41% enhanced QoL in IBS participants, and modulates the gut microbiome in healthy controls.

This review generates the hypothesis that routine physical activity may favorably alter gut microbiome composition in IBS to improve IBS symptomology. While a plausible hypothesis, research needs to confirm whether gut microbiome modulation is involved in physical activity associated IBS symptom relief.

Furthermore, the establishment of the most effective mode, duration, and intensity of physical activity for each sex and IBS-subtype is needed, with patient input during this process crucial to successfully translate science into practice.

Fish are exposed to numerous stressors which negatively affect their immune response and increase infection susceptibility. The risk of bacterial infections results in the excessive and preventive use of antibiotics. Therefore, we aimed to study how antibiotic treatment and restraint stress will affect the stress response, microbiota composition, gut morphology, and inflammatory reaction in common carp. Both restraint stress and antibiotic treatment increased cortisol level. Moreover, antibiotics induced dysbiosis in fish gut, manifested by a decrease in the total abundance of bacteria, and a shift in bacteria diversity, including a reduced number of Aeromonas, Bacteroides, Barnesiellaceae, Cetobacterium and Shewanella and an increased abundance of Flavobacterium. To a lesser extent, stress modified gut microbiota, as it decreased bacteria number and slightly changed the microbiota composition by decreasing Cetobacterium abundance and increasing Vibrio abundance. Microbiota of the antibiotic-treated and stressed fish shifted from the beneficial bacterial genera - Cetobacterium and Bacteroides, to the increased presence of unfavorable bacteria such as Brevinema, Flavobacterium and Desulfovibrionaceae. Stress and antibiotic-induced changes in the gut microbiota were related to the changes in the gut morphology when the higher abundance of goblet and rodlet cells and increased secretion activity of goblet cells were observed. Moreover, up-regulation of the expression of genes encoding pro-inflammatory mediators and cytokines involved in the Th17 immune response was present in the gut of the antibiotic-treated and stressed fish. We conclude that in carp antibiotics and stress alter the abundance and composition of the microbiota and induce Th17-dependent inflammatory reaction in the gut. Moreover, our results strongly suggest the interplay of the stress axis and the brain-gut-microbiota axis.

Lung cancer is a common malignant tumor worldwide with high incidence and mortality rates. Previous studies have claimed that the microbial community plays an integral role in the development and progression of lung cancer. Emerging evidence reveals that gut flora plays a key role in cancer formation and evolution by participating in mechanisms such as metabolism, regulation of inflammation and immune response. Not only the gut flora, but also the presence of intratumoral microbiota may influence lung cancer progression through multiple mechanisms. These research advances suggest that intestinal flora and intratumoral microbiota may not only serve as potential biomarkers for lung cancer, but may also be targets for therapy. However, current studies on both in lung cancer are still limited. Given this, this study aimed to systematically review the latest findings on the major bacterial species of the intestinal flora and their possible protective or harmful roles in the formation, progression, and metastasis of lung cancer. In addition, we analyzed the potential mechanisms by which the intratumoral microbiota affected lung cancer and elaborated on the potential roles of the gut flora and its metabolites, as well as the intratumoral microbiota, in modulating the efficacy of immunotherapy in lung cancer.

Microbiota modifiers offer potential benefits for improving the wide spectrum of symptoms and clinical outcomes in individuals with cancer. However, there is a lack of comprehensive literature mapping to determine which specific cancer and treatment-related symptoms have been investigated as potential targets for gut microbiota modifiers. This scoping review aims to systematically analyze clinical trials on microbiota modifiers in managing cancer and treatment-related symptoms in adults.

We conducted a scoping review of randomized controlled trials (RCTs) across four databases up to May 2025, following our published protocol and JBI principles with PRISMA 2020 guidelines.

The literature review identified 33 eligible studies, primarily involving patients with pelvic cancers. The most common outcomes examined in the clinical trials were gastrointestinal symptoms. Other studies focused on patients with head, neck, and breast cancer, examining quality of life, mucositis, fatigue, anxiety, depression, and the use of rescue drugs.

Despite evidence of potential benefits for gastrointestinal symptoms, inconsistent findings across studies warrant further well-designed, large-scale research to understand probiotics' effectiveness and mechanisms.

Osteoarthritis (OA) is a globally chronic disease affecting middle-aged and elderly individuals, with growing evidences implicating gut microbiota in its pathogenesis. Lactobacillus kefiranofaciens ZW3 (ZW3) shows potential in modulating gut microbiota, protecting intestinal barrier, and regulating immunity. This study explored the therapeutic effects of ZW3, alone and combined with CII/Gln, using a monoiodoacetate (MIA)-induced OA model. Results indicated that ZW3 significantly mitigated cartilage damage and inflammation alone or combined with CII/Gln, possibly by improving intestinal integrity, reduced oxidative stress, and regulated MMPs expression. 16S rDNA sequencing showed ZW3, especially with CII/Gln, increased beneficial bacteria of Ruminococcaceae and Lachnospiraceae abundances. Furthermore, ZW3 or with CII/Gln elevated SCFAs levels in intestinal contents in OA rats. These findings propose a novel probiotic-based strategy, potentially combined with functional foods, for OA intervention and treatment.

Heart failure (HF) remains a leading cause of morbidity and mortality worldwide, with inflammation playing a pivotal role in its pathogenesis. This comprehensive review aims to elucidate the intricate mechanisms by which inflammation contributes to the development and progression of HF. The review synthesizes current research on the involvement of both innate and adaptive immune responses in HF, highlighting the roles of cytokines, chemokines, and other inflammatory mediators. Recent studies have demonstrated that chronic inflammation, driven by factors such as oxidative stress, neurohormonal activation, and metabolic disturbances, leads to adverse cardiac remodeling and impaired myocardial function. The review explores how systemic inflammation, characterized by elevated levels of inflammatory biomarkers like C-reactive protein (CRP) and interleukin-6 (IL-6), correlates with HF severity and outcomes. Additionally, it discusses the impact of comorbid conditions such as diabetes, obesity, and hypertension on inflammatory pathways and HF risk. The review also delves into the therapeutic implications of targeting inflammation in HF. Despite mixed results from early clinical trials, emerging evidence suggests that anti-inflammatory therapies offer benefits in specific HF phenotypes. The potential of novel therapeutic strategies, including the use of biologics and small molecule inhibitors, is examined in the context of their ability to modulate inflammatory responses and improve clinical outcomes.

Intestinal health is crucial for digestive and absorptive functions, which are associated with fish growth performance. Searching for nutraceuticals and bioactive ingredients to improve intestinal health has become urgent for the aquaculture industry. In the present study, the effects of eicosapentaenoic acid (EPA) on intestinal function were investigated in turbot with induced intestinal damage caused by lipopolysaccharide (LPS). Juvenile turbot (initial weight 100 ± 5 g) were subjected to a 10-day enforced feeding regimen. Each fish was fed twice daily with either a 100 mg amino acid mixture (CON), an additional 1 mg of LPS (LPS), or an additional combination of 1 mg LPS and 1.7 mg EPA (LE). The results indicated that EPA supplementation restored intestinal villi integrity and the mucosal barrier. The number of goblet cells and the gene expression of MUC-2 were increased by EPA. Additionally, EPA suppressed the expression of inflammatory factors (MyD88 and NF-κB p65) and pro-inflammatory cytokines (TNFα, IL-1β, and IFN-γ). Meanwhile, post-feeding plasma free amino acid levels as well as intestinal protein synthesis were improved by EPA supplementation. The target of rapamycin (TOR) signaling pathway was significantly activated by EPA. Furthermore, EPA supplementation positively influenced intestinal microbiota, reducing the abundance of prevalent pathogens while enhancing the abundance of probiotics. Collectively, the administration of EPA effectively mitigates LPS-induced damage to the intestinal barrier, inflammatory response, and dysbiosis of microbiota through modulation of the TOR signaling pathway.

The intestinal microbiome is essential for gastrointestinal and overall health, yet its response to air pollution in children remains underexplored. In a study involving 412 young children from the ENVIRONAGE cohort, stool samples were analysed via Illumina Miseq sequencing to assess microbiome alpha diversity (observed richness, species evenness, and Shannon diversity) and composition. Exposure to previous year particulate air pollution (black carbon, PM2.5, coarse PM, and PM10) was modeled using high-resolution spatial-temporal interpolation models. Multiple linear regression models were adjusted for a priori selected covariables and stratified by sex. Furthermore, we performed a differential relative abundance analysis at family and genus level, while accounting for the same covariables. Statistically significant effect modification by sex was apparent for several intestinal alpha diversity indices and air pollutants. In boys, we observed negative associations between particulate air pollution exposure and intestinal microbiome richness (estimates ranging from -5.55 to -9.06 per interquartile range (IQR) increase in particulate air pollution exposure) and Shannon diversity (estimates ranging from -0.058 to -0.095 per IQR increase). Differently, in girls non-significant positive associations were observed with species evenness (estimates ranging from 0.019 to 0.020 per IQR increase) and Shannon diversity (estimate 0.065 per IQR increase in black carbon). After multiple testing correction, we reported several bacterial families and genera (Streptococcaceae, Clostridiales Incertae Sedis XIII, Coriobacteriaceae, Streptococcus, and Paraprevotella) to be oppositely associated with particulate air pollution exposure in boys and girls. Our findings show a sex-dependent association between particulate air pollution exposure and intestinal microbiome composition, highlighting boys as potentially more vulnerable to diversity loss associated with childhood exposure to particulate pollution.

Chronic metabolic inflammation is a common mechanism linked to the development of metabolic disorders such as obesity, diabetes, and cardiovascular disease (CVD). Chronic metabolic inflammation often related to alterations in gut homeostasis, and pathological processes involve the activation of endotoxin receptors, metabolic reprogramming, mitochondrial dysfunction, and disruption of intestinal nuclear receptor activity. Recent investigations into homeostasis and chronic metabolic inflammation have revealed a novel mechanism which is characterized by a timing interaction involving multiple components and targets. This article explores the positive impact of tea consumption on metabolic health of populations, with a special focus on the improvement of inflammatory indicators and the regulation of gut microbiota. Studies showed that tea consumption is related to the enrichment of gut microbiota. The relative proportion of Firmicutes/Bacteroidetes (F/B) is altered, while the abundance of Lactobacillus, Bifidobacterium, and A. muciniphila increased significantly in most of the studies. Thus, tea consumption could provide potential protection from the development of chronic diseases by improving gut homeostasis and reducing chronic metabolic inflammation. The direct impact of tea on intestinal homeostasis primarily targets lipopolysaccharide (LPS)-related pathways. This includes reducing the synthesis of intestinal LPS, inhibiting LPS translocation, and preventing the binding of LPS to TLR4 receptors to block downstream inflammatory pathways. The TLR4/MyD88/NF-κB p65 pathway is crucial for anti-metaflammatory responses. The antioxidant properties of tea are linked to enhancing mitochondrial function and mitigating mitochondria-related inflammation by eliminating free radicals, inhibiting NLRP3 inflammasomes, and modulating Nrf2/ARE activity. Tea also contributes to safeguarding the intestinal barrier through various mechanisms, such as promoting the synthesis of short-chain fatty acids in the intestine, activating intestinal aryl hydrocarbon receptor (AhR) and farnesoid X receptor (FXR), and improving enteritis. Functional components that improve chronic metabolic inflammation include tea polyphenols, tea pigments, TPS, etc. Tea metabolites such as 4-Hydroxyphenylacetic acid and 3,4-Dihydroxyflavan derivatives, etc., also contribute to anti-chronic metabolic inflammation effects of tea consumption. The raw materials and processing technologies affect the functional component compositions of tea; therefore, consuming different types of tea may result in varying action characteristics and mechanisms. However, there is currently limited elaboration on this aspect. Future research should conduct in-depth studies on the mechanism of tea and its functional components in improving chronic metabolic inflammation. Researchers should pay attention to whether there are interactions between tea and other foods or drugs, explore safe and effective usage and dosage, and investigate whether there are individual differences in the tea-drinking population leading to different effects of tea intervention. Ultimately, the application of tea drinking could be a universal therapy for regulating intestinal homeostasis, anti-chronic metabolic inflammatory responses, and promoting metabolic health.

The human gut microbiome represents a complex ecosystem comprising numerous microorganisms critical to basic physiological processes. The gut microbiome's composition and functionality influence surgical outcomes following orthopedic procedures. The purpose of this study was to evaluate the gut microbiota on critical aspects of orthopedic surgical outcomes. A comprehensive literature search was conducted via PubMed, the Cumulative Index for Nursing and Allied Health Literature (CINAHL), Google Scholar, Cochrane Library, Medline, and Web of Science. A total of 18 research articles of the 599 retrieved results were included in this study. Significant correlations were identified between microbial composition and surgical outcomes, including infection rates, inflammatory responses, and postoperative complications. Bacterial genera like Alistipes and Helicobacter increased postoperative cognitive dysfunction (POCD) risk, while short-chain fatty acid (SCFA)-producing bacteria showed negative correlations with inflammatory markers. Probiotic interventions reduced POCD incidence from 16.4% to 5.1% and modulated inflammatory responses. Additionally, bacterial composition was associated with critical surgical parameters such as bone healing, infection rate, and recovery trajectory. Inflammation, healing processes, and recovery trajectories are influenced by microbial composition in surgical settings. Targeted interventions, such as probiotics, show promise in reducing surgical risks and improving patient recovery.

From a biological point of view, Diversity, Equity, and Inclusion (DEI) are important at multiple levels, which include our genetics, microbiomes, diets, and all organ system interactions. Considering only DEI's sociological aspects is equivalent to the error of "throwing out the baby with the bath water." Variances in microbial diversity within our microbiomes might affect our health through systemic interactions affecting metabolites, maintaining immune homeostasis, and wound healing of cellular damage from an infection, physical stress, or psychological trauma. An imbalance of our immune cell subsets, both innate and adaptive, and the microbes in any of our microbiomes might lead to more cellular damage from excessive inflammation and oxidative stress and less immune regulation. The immune dysregulation may occur due to the loss of endometrial barriers enabling the spread of microbes, environmental pollutants, and allergens. Heat waves, sleep deprivation, and increased prevalence of pollutants such as polychlorinated biphenyls, which weaken endothelial barriers, may be responsible for the enhanced prevalence of physical and psychological stresses. Leakage of our useful gut microbiota into the periphery might initiate inflammatory responses, and an altered gut microbiome might affect the gut-brain axis that influences physical and mental health.

The complex nature of immune system behavior in both autoimmune diseases and transplant rejection can be understood through the lens of avalanche dynamics in critical-point systems. This paper introduces the concept of the "immunological avalanche" as a framework for understanding unpredictable patterns of immune activity in both contexts. Just as avalanches represent sudden releases of accumulated potential energy, immune responses exhibit periods of apparent stability followed by explosive flares triggered by seemingly minor stimuli. The model presented here draws parallels between immune system behavior and other complex systems such as earthquakes, forest fires, and neuronal activity, where localized events can propagate into large-scale disruptions. In autoimmune conditions like systemic lupus erythematosus (SLE), which affects multiple organ systems including the kidneys in approximately 50% of patients, these dynamics manifest as alternating periods of remission and flares. Similarly, in transplant recipients, the immune system exhibits metastable behavior under constant allograft stimulation. This critical-point dynamics framework is characterized by threshold-dependent activation, positive feedback loops, and dynamic non-linearity. In autoimmune diseases, triggers such as UV light exposure, infections, or stress can initiate cascading immune responses. In transplant patients, longitudinal analysis reveals how monitoring oscillatory patterns in blood parameters and biological age markers can predict rejection risk. In a preliminary study on kidney transplant, all measured variables showed temporal instability. Proteinuria exhibited precise log-log linearity in power law analysis, confirming near-critical-point system behavior. Two distinct dynamic patterns emerged: large oscillations in eGFR, proteinuria, or biological age predicted declining function, while small oscillations indicated stability. During avalanche events, biological age increased dramatically, with partial reversal leaving persistent elevation after acute episodes. Understanding these dynamics has important implications for therapeutic approaches in both contexts. Key findings suggest that monitoring parameter oscillations, rather than absolute values, better indicates system instability and potential avalanche events. Additionally, biological age calculations provide valuable prognostic information, while proteinuria measurements offer efficient sampling for system dynamics assessment. This conceptual model provides a unifying framework for understanding the pathogenesis of both autoimmune and transplant-related immune responses, potentially leading to new perspectives in disease management and rejection prediction.

Nonalcoholic Steatohepatitis (NASH) is a progressive liver disease characterized by inflammation and liver damage. Allicin, a bioactive compound derived from garlic, has demonstrated anti-inflammatory and antioxidant properties. This study explores the effects of allicin on NASH and gut microbiota dysbiosis induced by a high-fat, high-fructose diet (HFFD) in mice. Allicin supplementation significantly alleviated hepatic inflammation, improved glucose metabolism, and modulated the circadian rhythm gene Rev-erbα, which plays a critical role in regulating inflammation. The anti-inflammatory effects of allicin were diminished in Si-Rev-erbα-treated HepG2 cells, highlighting the importance of circadian regulation in mediating these effects. Allicin's anti-inflammatory effects were associated with increased levels of short-chain fatty acids (SCFAs) and the restoration of diurnal oscillations in proinflammatory cytokines and gut microbiota composition, particularly in genera, such as Akkermansia, Bacteroidetes, and Lactobacillus. These findings suggest that allicin could be a promising therapeutic approach for managing NASH, liver dysfunction, and related metabolic disorders through the modulation of circadian rhythms and the gut microbiome.

This narrative review presents the role of antioxidants in regulating the gut microbiota and the impact on the gut-brain axis, with a particular focus on neurodegenerative diseases, such as Alzheimer's (AD) and Parkinson's disease (PD). These diseases are characterised by cognitive decline, motor dysfunction, and neuroinflammation, all of which are significantly exacerbated by oxidative stress. This review elucidates the contribution of oxidative damage to disease progression and explores the potential of antioxidants to mitigate these pathological processes through modulation of the gut microbiota and associated pathways. Based on recent studies retrieved from reputable databases, including PubMed, Web of Science, and Scopus, this article outlines the mechanisms by which antioxidants influence gut health and exert neuroprotective effects. Specifically, it discusses how antioxidants, including polyphenols, vitamins, and flavonoids, contribute to the reduction in reactive oxygen species (ROS) production and neuroinflammation, thereby promoting neuronal survival and minimising oxidative damage in the brain. In addition, the article explores the role of antioxidants in modulating key molecular pathways involved in oxidative stress and neuroinflammation, such as the NF-κB, Nrf2, MAPK, and PI3K/AKT pathways, which regulate ROS generation, inflammatory cytokine expression, and antioxidant responses essential for maintaining cellular homeostasis in both the gut and the central nervous system. In addition, this review explores the complex relationship between gut-derived metabolites, oxidative stress, and neurodegenerative diseases, highlighting how dysbiosis-an imbalance in the gut microbiota-can exacerbate oxidative stress and contribute to neuroinflammation, thereby accelerating the progression of such diseases as AD and PD. The review also examines the role of short-chain fatty acids (SCFAs) produced by beneficial gut bacteria in modulating these pathways to attenuate neuroinflammation and oxidative damage. Furthermore, the article explores the therapeutic potential of microbiota-targeted interventions, including antioxidant delivery by probiotics and prebiotics, as innovative strategies to restore microbial homeostasis and support brain health. By synthesising current knowledge on the interplay between antioxidants, the gut-brain axis, and the molecular mechanisms underlying neurodegeneration, this review highlights the therapeutic promise of antioxidant-based interventions in mitigating oxidative stress and neurodegenerative disease progression. It also highlights the need for further research into antioxidant-rich dietary strategies and microbiota-focused therapies as promising avenues for the prevention and treatment of neurodegenerative diseases.

The concept of the gut microbes-muscle axis underscores the impact of intestinal microbiota on the muscular system, an area that is increasingly coming to light. However, current interpretations and applications of this concept remain underdeveloped. In this review, we concluded and discussed factors, such as short-chain fatty acids, amino acids, vitamins, bile acids, antibiotics, cytokines, hormones, and extracellular vesicles that mediate gut microbes-muscle crosstalk and influence the gut microbes-muscle axis. Additionally, we examined how the gut microbes-muscle axis affects muscle mass, muscle strength, muscle metabolism, as well as muscle oxidative and immune status. Furthermore, we reviewed the influence of the microbes-muscle axis on muscle fiber type transition, muscle fat deposition, and meat quality. These insights illuminate the potential mechanisms by which the gut microbes-muscle axis operates in humans and animals. Thus, this review provides a theoretical foundation for future research and offers practical guidance for its application in biomedical and livestock industries.

This editorial comments on the article by Wu et al in the World Journal of Gastroenterology. The article explored the relationship between mesenteric adipose tissue, creeping fat, inflammation, and gut microbiota in Crohn's disease (CD). We discussed three key aspects of the interaction between gut microbiota and inflammatory bowel disease (IBD): The physiological functions of the gut microbiota, the potential role of probiotics in IBD treatment; and the effect of fecal microbiota transplantation (FMT) in combating IBD. IBD, comprising CD and ulcerative colitis (UC), is influenced by the gut microbiota. Changes in gut microbiota composition disrupt intestinal function and promote chronic inflammation, but the exact mechanisms remain unclear. Probiotics have demonstrated some efficacy in inducing remission in UC, though their effectiveness in CD is still debated. FMT shows promise in treating IBD, especially UC, by restoring gut microbiota diversity and inducing clinical remission. As for CD, FMT has potential, but more studies are needed to confirm its long-term effectiveness and safety. Dietary approaches may help manage IBD symptoms or disease activity, but patient adherence is crucial. Clinicians and researchers must recognize the importance of the gut microbiota and the need for personalized therapies targeting microbial imbalances.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in social communication and behavior, frequently accompanied by restricted and repetitive patterns of interests or activities. The gut microbiota has been implicated in the etiology of ASD due to its impact on the bidirectional communication pathway known as the gut-brain axis. However, the precise involvement of the gut microbiota in the causation of ASD is unclear. This study critically examines recent evidence to rationalize a probable mechanism in which gut microbiota symbiosis can induce neuroinflammation through intermediator cytokines and metabolites. To develop ASD, loss of the integrity of the intestinal barrier, activation of microglia, and dysregulation of neurotransmitters are caused by neural inflammatory factors. It has emphasized the potential role of neuroinflammatory intermediates linked to gut microbiota alterations in individuals with ASD. Specifically, cytokines like brain-derived neurotrophic factor, calprotectin, eotaxin, and some metabolites and microRNAs have been considered etiological biomarkers. We have also overviewed how probiotic trials may be used as a therapeutic strategy in ASD to reestablish a healthy balance in the gut microbiota. Evidence indicates neuroinflammation induced by dysregulated gut microbiota in ASD, yet there is little clarity based on analysis of the circulating immune profile. It deems the repair of microbiota load would lower inflammatory chaos in the GI tract, correct neuroinflammatory mediators, and modulate the neurotransmitters to attenuate autism. The interaction between the gut and the brain, along with alterations in microbiota and neuroinflammatory biomarkers, serves as a foundational background for understanding the etiology, diagnosis, prognosis, and treatment of autism spectrum disorder.

Age-related macular degeneration (AMD) is a multifactorial disease, and studies have implicated the role of gut microbiota in its pathogenesis. However, characterization of microbiome dysbiosis and associated microbial-derived metabolomic profiles across AMD stages remains unknown. In this pilot study, we explored how gut microbiome composition and gut-derived metabolites differ in AMD.

Our pilot study analyzed fasted stool samples that were collected from 22 patients at a tertiary academic center. Subjects were classified as control, intermediate AMD, or advanced AMD based on clinical presentation. 16S rRNA amplicon sequencing and standard chromatography-mass spectrometry methods were used to identify bacterial taxonomy composition and abundance of short-chain fatty acids (SCFAs) and bile acids (BAs), respectively. Genetic testing was used to investigate the frequency of 14 high-risk single nucleotide polymorphisms (SNPs) associated with AMD in the AMD cohort.

Forty-three differentially abundant genera were present among the control, intermediate, and advanced groups. Taxa with known roles in immunologic pathways, such as Desulfovibrionales (q = 0.10) and Terrisporobacter (q = 1.16e-03), were in greater abundance in advanced AMD patients compared to intermediate. Advanced AMD patients had decreased abundance of 12 SCFAs, including acetate (P = 0.002), butyrate (P = 0.04), and propionate (P = 0.01), along with 12 BAs, including taurocholic acid (P = 0.02) and tauroursodeoxycholic acid (P = 0.04). Frequencies of high-risk SNPs were not significantly different between the intermediate and advanced AMD groups.

This pilot study identifies distinct gut microbiome compositions and metabolomic profiles associated with AMD and its stages, providing preliminary evidence of a potential link between gut microbiota and AMD pathogenesis. To validate these findings and elucidate the underlying mechanisms, future research with larger cohorts and more comprehensive sampling is strongly recommended.

Extensive research indicates a link between gut microbiota dysbiosis and psychiatric disorders. However, the causal relationships between gut microbiota and different types of psychiatric disorders, as well as whether inflammatory factors mediate these relationships, remain unclear.

We utilized summary statistics from the largest genome-wide association studies to date for gut microbiota (n = 18,340 in MiBioGen consortium), circulating inflammatory factors (n = 8293 for 41 factors and n = 14,824 for 91 factors in GWAS catalog), and six major psychiatric disorders from the Psychiatric Genomics Consortium (PGC): attention deficit hyperactivity disorder (ADHD, n = 38,691), anxiety disorder (ANX, n = 2248), bipolar disorder (BIP, n = 41,917), anorexia nervosa (AN, n = 16,992), schizophrenia (SCZ, n = 36,989), and autism spectrum disorder (ASD, n = 18,381). We conducted bidirectional Mendelian randomization (MR) analysis to explore the causal relationships between gut microbiota and psychiatric disorders. Additionally, we performed two-step MR and multivariable MR (MVMR) analyses to identify potential mediating inflammatory factors.

We found significant causal relationships between 11 gut microbiota and ADHD, 2 gut microbiota and ANX, 11 gut microbiota and BIP, 8 gut microbiota and AN, 15 gut microbiota and SCZ, and 5 gut microbiota and ASD. There were 16 positive and 15 negative causal effects between inflammatory factors and psychiatric disorders. Furthermore, MVMR analysis results indicated that the correlation between genus Roseburia and ADHD was mediated by MCSF, with a mediation proportion of 3.3 %; the correlation between genus Erysipelotrichaceae UCG003 and BIP was mediated by GDNF, with a mediation proportion of 3.7 %; and the correlation between family Prevotellaceae and SCZ was mediated by CD40, with a mediation proportion of 8.2 %.

The MR analysis results supported causal relationships between gut microbiota and six psychiatric disorders, as well as the potential mediating role of inflammatory factors. This study highlights the potential role of the gut microbiota-inflammation-brain axis in psychiatric disorders.

Artificial sweeteners have emerged as popular alternatives to traditional sweeteners, driven by the growing concern over sugar consumption and its associated rise in obesity and metabolic disorders. Despite their widespread use, the safety and health implications of artificial sweeteners remain a topic of debate, with conflicting evidence contributing to uncertainty about their long-term effects. This review synthesizes current scientific evidence regarding the impact of artificial sweeteners on gut microbiota and gastrointestinal health. Our analysis of in vitro experiments, animal models, and clinical trials reveals that artificial sweeteners can alter the composition and abundance of gut microbes. These changes raise concerns about their potential to affect overall gut health and contribute to gastrointestinal disorders. Additionally, artificial sweeteners have been shown to influence the production of metabolites by gut bacteria, further impacting systemic health. The findings suggest that artificial sweeteners may have complex and sometimes contradictory effects on gut microbiota. While some studies indicate potential benefits, such as reduced caloric intake and weight management, others highlight detrimental effects on microbial balance and metabolic functions. The inconsistent results underscore the need for further research to comprehensively understand the physiological impacts of various artificial sweeteners on human health. Future studies should aim for long-term, well-controlled investigations to clarify these relationships, ensuring evidence-based guidelines for the safe use of artificial sweeteners in diet management. © 2025 Society of Chemical Industry.

Background: Periprosthetic joint infections (PJIs) pose a significant challenge in orthopedic surgery, and emerging evidence suggests that the gut microbiome may play a crucial role in their development and management. Despite the rarity of these infections, the continuous increase in prosthetic joint arthroplasties has made understanding how to prevent them more pressing. A stronger comprehension of the disruption of the gut microbiome and how this can lead to more of these infections and other pre-surgical risks may be crucial in preventing them. Objective: This article aims to provide a stronger understanding of the topic through the analysis of different pieces of already existing literature to help draw new conclusions and raise potential questions that need answering. Methods: A comprehensive search strategy without filters was employed, and multiple papers were thoroughly analyzed, understood, and compiled into this paper. Conclusions: Despite the limitations of some of the analyzed studies and finite evidence, this paper suggests that there could be a connection between periprosthetic joint infections and a compromised gut microbiome. However, further research is required to draw a definitive conclusion.

Postbiotics may help strengthen intestinal barrier function. This study assessed the effects of a postbiotic derived from Limosilactobacillus fermentum and Lactobacillus delbrueckii subsp. lactis on epithelial barrier and cytokine production. Human-derived colon tubules were cultured on chips for 15 days. On day 8, the epithelial barrier was disrupted with 0.7 μM afatinib. Postbiotic doses of 5, 10, or 20 mg/mL were added on days 6, 8, 11, and 13. Trans-epithelial electrical resistance (TEER) was measured on days 6, 8, 11, 13, and 15, along with phase contrast imaging. Cytokine levels were measured on day 13. All three postbiotic concentrations resulted in better TEER recovery on day 15 vs. the control (p < 0.001). On day 13, 10 and 20 mg/mL increased TEER (p < 0.001), but only 20 mg/mL did on day 11 (p < 0.05). Phase imaging confirmed the dose-dependent effect. The 20 mg/mL dose more effectively reduced CCL2, CX3CL1, CXCL1, CXCL5, IL-8, IL-11, and IL-4 than the other doses (p < 0.01), and 10 mg/mL more effectively reduced CCL2, CXCL1, CXCL10, IL-10, IL-11, and IL-23 than 5 mg/mL (p < 0.01). In a colonic organoid model, the Lactobacillaceae-derived postbiotic prevented drug-induced epithelial damage, enhanced recovery, and modulated cytokine secretion towards a more anti-inflammatory profile in a dose-dependent manner.

Gastrointestinal homeostasis describes a delicate state of equilibrium in which various systems cooperate to maintain digestive health, support microbial activity, and regulate immune responses. There is growing evidence that Vitamin D is one of the many factors that influences gastrointestinal homeostasis through its effects on gut barrier integrity, regulating microbial diversity and modulating immune responses. Given these effects of Vitamin D, there may be potential for it as both a preventative and a therapeutic intervention for a variety of conditions, but especially for inflammatory conditions of the gastrointestinal tract. This article will summarize the role of Vitamin D in a state of equilibrium, as well as its role in a pro-inflammatory state in the gastrointestinal tract.

Numerous factors are involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), which are responsible for its development and progression as an independent entity, but also thanks to their simultaneous action. This is explained by the hypothesis of multiple parallel hits. These factors are insulin resistance, lipid metabolism alteration, oxidative stress, endoplasmic reticulum stress, inflammatory cytokine liberation, gut microbiota dysbiosis or gut-liver axis activation. This is a systematic review which has an aim to show the connection between intestinal microbiota and the role of its disbalance in the development of NAFLD. The gut microbiota is made from a wide spectrum of microorganisms that has a systemic impact on human health, with a well-documented role in digestion, energy metabolism, the stimulation of the immune system, synthesis of essential nutrients, etc. It has been shown that dysbiosis is associated with all three stages of chronic liver disease. Thus, the modulation of the gut microbiota has attracted research interest as a novel therapeutic approach for the management of NAFLD patients. The modification of microbiota can be achieved by substantial diet modification and the application of probiotics or prebiotics, while the most radical effects are observed by fecal microbiota transplantation (FMT). Given the results of FMT in the context of metabolic syndrome (MetS) and NAFLD in animal models and scarce pilot studies on humans, FMT seems to be a promising treatment option that could reverse intestinal dysbiosis and thereby influence the course of NAFLD.

Inflammatory bowel disease (IBD) is a chronic condition that includes two main types, Crohn's disease (CD) and ulcerative colitis (UC), involving inflammation of the gastrointestinal (GI) tract. The exact cause of IBD is unknown but could be a combination of genetic, environmental, and immune system factors. This study investigated the impact of IBD on microbiota diversity by evaluating the differences in microbial composition and the microbiota of a control group (A) of healthy individuals and a group (B) of IBD patients. Sixty biopsies were collected from participants recruited from hospitals in Makkah, Saudi Arabia. Biopsy specimens were taken during colonoscopy examination, and bacterial identification was performed by extracting ribosomal DNA from sigmoid colon biopsies using a DNeasy Blood & Tissue Kit. Metagenomics and bioinformatics analyses were then conducted to analyze and compare the microbiota in the two groups. The results showed that the varieties of core microbiome species were 3.81% greater in the IBD patients than in the members of the control group. Furthermore, the differences between the groups were significantly greater than the variations within each group. Differences between the two groups were detected in the relative abundance of Clostridium nexile, Ruminococcus gnavus, Ruminococcus faecis, and Escherichia coli. These results indicate that microbiota could play a role in the pathogenesis of IBD and suggest that microbial diversity can serve as a biomarker for diagnosing the disease and monitoring its progression.

Over the last few decades, the prevalence of metabolic diseases such as obesity, diabetes, non-alcoholic fatty liver disease, hypertension, and hyperuricemia has surged, primarily due to high-fat diet (HFD). The pathologies of these metabolic diseases show disease-specific alterations in the composition and function of their gut microbiome. How HFD alters the microbiome and its metabolite to mediate adipose tissue (AT) inflammation and obesity is not well known. Thus, this study aimed to identify the changes in the gut microbiome and metabolomic signatures induced by an HFD to alter obesity. To explore the changes in the gut microbiota and metabolites, 16S rRNA gene amplicon sequencing and metabolomic analyses were performed after HFD and normal diet (ND) feeding. We noticed that, at taxonomic levels, the number of operational taxonomic units (OTUs), along with the Chao and Shannon indexes, significantly shifted in HFD-fed mice compared to those fed a ND. Similarly, at the phylum level, an increase in Firmicutes and a decrease in Bacteroidetes were noticed in HFD-fed mice. At the genus level, an increase in Lactobacillus and Ruminococcus was observed, while Allobaculum, Clostridium, and Akkermansia were markedly reduced in the HFD group. Many bacteria from the Ruminococcus genus impair bile acid metabolism and restrict weight loss. Firmicutes are efficient in breaking down complex carbohydrates into short-chain fatty acids (SCFAs) and other metabolites, whereas Bacteroidetes are involved in a more balanced or efficient energy extraction. Thus, an increase in Firmicutes over Bacteroidetes enhances the absorption of more calories from food, which may contribute to obesity. Taken together, the altered gut microbiota and metabolites trigger AT inflammation, which contributes to metabolic dysregulation and disease progression. Thus, this study highlights the potential of the gut microbiome in the development of therapeutic strategies for obesity and related metabolic disorders.

Oncologists increasingly recognize the microbiome as an important facilitator of health as well as a contributor to disease, including, specifically, cancer. Our knowledge of the etiologies, mechanisms, and modulation of microbiome states that ameliorate or promote cancer continues to evolve. The progressive refinement and adoption of "omic" technologies (genomics, transcriptomics, proteomics, and metabolomics) and utilization of advanced computational methods accelerate this evolution. The academic cancer center network, with its immediate access to extensive, multidisciplinary expertise and scientific resources, has the potential to catalyze microbiome research. Here, we review our current understanding of the role of the gut microbiome in cancer prevention, predisposition, and response to therapy. We underscore the promise of operationalizing the academic cancer center network to uncover the structure and function of the gut microbiome; we highlight the unique microbiome-related expert resources available at the City of Hope of Comprehensive Cancer Center as an example of the potential of team science to achieve novel scientific and clinical discovery.

Alzheimer's Disease (AD) is a debilitating neurocognitive disorder with an unclear underlying mechanism. Recent studies have implicated gut microbiota dysbiosis with the onset and progression of AD. The connection between gut microbiota and AD can significantly affect the prevention and treatment of AD patients. This systematic review summarizes primary outcomes of human and mouse AD models concerning gut microbiota alterations. A systematic literature search in February through March 2023 was conducted on PubMed, Embase, and Web of Science. We identified 711 as potential manuscripts of which 672 were excluded because of irrelevance to the identified search criteria. Primary outcomes include microbiota compositions of control and AD models in humans and mice. In total, 39 studies were included (19 mouse and 20 human studies), published between 2017 and 2023. We included studies involving well-established mice models of AD (5xFAD, 3xTg-AD, APP/PS1, Tg2576, and APPPS2) which harbor mutations and genes that drive the formation of Aß plaques. All human studies were included on those with AD or mild cognitive impairment. Among alterations in gut microbiota, most studies found a decreased abundance of the phyla Firmicutes and Bifidobacteria, a genus of the phylum Actinomycetota. An increased abundance of the phyla Bacteroidetes and Proteobacteria were identified in animal and human studies. Studies indicated that gut microbiota alter the pathogenesis of AD through its impact on neuroinflammation and permeability of the gastrointestinal tract. The ensuing increase in blood-brain barrier permeability may accelerate Aβ penetrance and formation of neuritic plaques that align with the amyloid hypothesis of AD pathogenesis. Further studies should assess the relationship between gut microbiota and AD progression and therapy preserving beneficial gut microbiota.

The gut microbiome, a complex ecosystem of microorganisms, plays a pivotal role in human health and disease. The gut microbiome's influence extends beyond the digestive system to various organs, and its imbalance is linked to a wide range of diseases, including cancer and neurodevelopmental, inflammatory, metabolic, cardiovascular, autoimmune, and psychiatric diseases. Despite its significance, the interactions between gut bacteria and human proteins remain understudied, with less than 20,000 experimentally validated protein interactions between the host and any bacteria species. This study addresses this knowledge gap by predicting a protein-protein interaction network between gut bacterial and human proteins. Using statistical associations between Pfam domains, a comprehensive dataset of over one million experimentally validated pan-bacterial-human protein interactions, as well as inter- and intra-species protein interactions from various organisms, were used for the development of a machine learning-based prediction method to uncover key regulatory molecules in this dynamic system. This study's findings contribute to the understanding of the intricate gut microbiome-host relationship and pave the way for future experimental validation and therapeutic strategies targeting the gut microbiome interplay.

The human microbiota, a complex ecosystem of microorganisms, plays a pivotal role in regulating host immunity and metabolism. This review investigates the interplay between microbiota and inflammatory markers, emphasizing their impact on metabolic and autoimmune disorders. Key inflammatory biomarkers, such as C-reactive protein (CRP), interleukin-6 (IL-6), lipopolysaccharides (LPS), zonulin (ZO-1), and netrin-1 (Ntn1), are discussed in the context of intestinal barrier integrity and chronic inflammation. Dysbiosis, characterized by alterations in microbial composition and function, directly modulates the levels and activity of these biomarkers, exacerbating inflammatory responses and compromising epithelial barriers. The disruption of microbiota is further correlated with increased intestinal permeability and chronic inflammation, serving as a precursor to conditions like type 2 diabetes (T2D), obesity, and non-alcoholic fatty liver disease. Additionally, this review examines therapeutic strategies, including probiotics and prebiotics, designed to restore microbial balance, mitigate inflammation, and enhance metabolic homeostasis. Emerging evidence positions microbiota-targeted interventions as critical components in the advancement of precision medicine, offering promising avenues for diagnosing and treating inflammatory and metabolic disorders.

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.

Prenatal and postpartum depression may be influenced by the composition of host associated microbiomes. As such, the objective of this study was to elucidate the relationship between the human gut or vaginal microbiomes in pregnancy with prenatal or postpartum depression.

140 female participants were recruited at their first prenatal visit and completed the Edinburgh Postnatal Depression Scale (EPDS) to screen for depression and anxiety, in addition the EPDS was completed one month postpartum. Vaginal and stool biospecimens were collected in the third trimester, analyzed using 16S rRNA gene sequencing, and assessed for alpha and beta diversity. Individual taxa differences and clustering using the k-medoids algorithm enabled community state type classification.

Participants with higher postpartum EPDS scores had higher species richness and lower abundance of L. crispatus in the vaginal microbiota compared to those with lower EPDS scores. Participants with a higher prenatal EPDS score had lower species richness of the gut microbiome. Participants with a vaginal community state type dominated by L. iners had the highest mean prenatal EPDS scores, whereas postpartum EPDS scores were similar regardless of prenatal vaginal state type.

Our small sample size and participant's self-report bias limits generalizability of results.

Depression in the prenatal and postpartum period is associated with the composition and diversity of the gut and vaginal microbiomes in the third trimester of pregnancy. These results provide a foundational understanding of the microbial relationships between maternal health and depression for identifying potential therapeutic treatments.

Sedentarism is characterized by low levels of physical activity, a risk factor for obesity and cardio-metabolic diseases. It can also adversely affect the composition and diversity of the gut microbiome which may result in harmful consequences for human health. While cardiorespiratory fitness (CRF) is inversely and independently associated with cardiovascular risk factors and diseases and all-cause mortality, the relationship between low CRF and the gut microbiome is not well known. A total of 3,616 individuals from two independent population-based cohorts of the Study of Health in Pomerania (SHIP-START and SHIP-TREND) performed standardized, symptom-limited cardiopulmonary exercise testing (CPET) and had faecal samples collected to determine gut microbiota profiles (16S rRNA gene sequencing). We analysed cross-sectional associations of CRF with the gut microbiome composition controlling for confounding factors. Lower CRF was associated with reduced microbial diversity, loss of beneficial short-chain fatty acid producing bacteria (i.e. Butyricoccus, Coprococcus, unclassified Ruminococcaceae or Lachnospiraceae) and an increase in opportunistic pathogens such as Escherichia/Shigella, or Citrobacter. Decreased cardiorespiratory performance was associated with a gut microbiota pattern that has been previously related to a proinflammatory state. These associations were independent of body weight or glycemic control.

The gut microbiota is known to interact with various organs in the body, including the central nervous system, through the gut-brain axis. Intestinal dysbiosis can lead to increased peripheral inflammation and, consequently, affect the brain, resulting in neuroinflammation. Photobiomodulation (PBM) has demonstrated positive regulatory effects on the imbalance of certain body functions, including pain, inflammation, immunity, wound healing, and gut microbiota dysbiosis. Therefore, PBM at the intestinal level could help improve intestinal dysbiosis and reestablish cerebral homeostasis. In this context, this study aimed to conduct a narrative review of the literature on the effects of PBM at the intestinal level on intestinal dysbiosis and neuroinflammation. Overall, the findings highlight that PBM modulates the gut microbiota, suggesting it could serve as a therapy for neurological conditions affecting the gut-brain axis. Future research should focus on further elucidating the molecular mechanisms underlying this therapy.

Knowledge about the association between oral microbiome diversity within individuals and cardiovascular disease (CVD) and non-CVD mortality is scarce. Besides, variation by sex and racial and ethnic groups, and the potential mediators of these associations remain unclear. We aimed to investigate the associations of oral microbiome alpha diversity with all-cause, CVD, and non-CVD mortality, and the interaction effects of sex and racial and ethnic groups and potential mediators in the associations.

The National Health and Nutrition Examination Survey (NHANES) is a population-based observational study, conducted periodically in Mexican American, Other Hispanic, Non-Hispanic (NH) White, NH Black, and other racial/ethnic participants. We linked 2009-12 survey data of 8199 adults to the mortality data until 2019. By analyzing RNA gene sequences from oral rinse samples, microbiome alpha diversity within individuals was assessed using operational taxonomic unit (OTU) richness. Potential mediators included obesity, diabetes mellitus, dyslipidemia, hypertension, and periodontitis. Multivariable Cox proportional hazards regression and causal mediation analysis were used.

Baseline mean ± standard deviation (SD) age was 42.1 ± 15.1 years. Over a median follow-up of 9.1 years, 405 all-cause mortality occurred (CVD, 105; non-CVD, 300). Each 1-SD increment in OTU richness was inversely associated with all-cause mortality (hazard ratio [HR] 0.92, 95 % confidence interval [CI] 0.90-0.95), CVD mortality (HR, 0.92; 95 % CI, 0.90-0.95), and non-CVD mortality (HR, 0.92; 95 % CI, 0.90-0.95). With evidence of significant racial and ethnic groups-interaction (p <0.05), these associations were evident in Mexican American, NH White, and others racial/ethnic participants. None of the potential mediators significantly mediated the associations of OTU richness with all-cause, CVD, and non-CVD mortality.

Lower oral microbiome alpha diversity is associated with higher risk for all-cause, CVD, and non-CVD mortality, and the associations are varied by racial and ethnic groups.

Increasing prevalence of childhood obesity has emerged as a critical global public health concern. Recent studies have challenged the previous belief that obesity was solely a result of excessive caloric intake. Alterations in early-life gut microbiota can contribute to childhood obesity through their influence on nutrient absorption and metabolism, initiation of inflammatory responses, and regulation of gut-brain communication. The gut microbiota is increasingly acknowledged to play a crucial role in human health, as certain beneficial bacteria have been scientifically proven to possess the capacity to reduce body fat content and enhance intestinal barrier function and their metabolic products to exhibit anti-inflammatory effect. Examples of such microbes include bifidobacteria, Akkermansia muciniphila, and Lactobacillus reuteri. In contrast, an increase in Enterobacteriaceae and propionate-producing bacteria (Prevotellaceae and Veillonellaceae) has been implicated in the induction of low-grade systemic inflammation and disturbances in lipid metabolism, which can predispose individuals to obesity. Studies have demonstrated that modulating the gut microbiota through diet, lifestyle changes, prebiotics, probiotics, or fecal microbiota transplantation may contribute to gut homeostasis and the management of obesity and its associated comorbidities. This review aimed to elucidate the impact of alterations in gut microbiota composition during early life on childhood obesity and explores the mechanisms by which gut microbiota contributes to the pathogenesis of obesity and specifically focused on recent advances in using short-chain fatty acids for regulating gut microbiota and ameliorating obesity. Additionally, it aimed to discuss the therapeutic strategies for childhood obesity from the perspective of gut microbiota, aiming to provide a theoretical foundation for interventions targeting pediatric obesity based on gut microbiota.

Macrophages are members of the human innate immune system, and the majority reside in the liver. In recent years, they have been recognized as essential players in the maintenance of liver and intestinal homeostasis as well as key guardians of their respective immune systems, and they are increasingly being recognized as such. Paradoxically, they are also likely involved in chronic pathologies of the gastrointestinal tract and potentially in the alteration of the gut-liver axis in alcohol use disorder (AUD) and alcohol-associated liver disease (ALD). To date, the causal relationship between macrophages, the pathogenesis of ALD, and the immune dysregulation of the gut remains unclear. In this review, we will discuss our current understanding of the heterogeneity of intestinal and hepatic macrophages, their ontogeny, the potential factors that regulate their origin, and the evidence of how they are associated with the manifestation of chronic inflammation. We will also illustrate how the micro-environment of the intestine shapes the phenotypes and functionality of the macrophage compartment in both the intestines and liver and how they change during chronic alcohol abuse. Finally, we highlight the obstacles to current research and the prospects for this field.

This systematic review explores the associations between qualitative/quantitative changes in gut microbiota and psychopathological symptoms or other clinical features in patients with eating disorders (EDs). Secondary outcomes include exploring gut microbiota changes in EDs and potential relationships with psychotropic drug use.

A systematic search was conducted across biomedical databases from inception to June 2024 according to PRISMA guidelines. The risk of bias was assessed, and a narrative synthesis was performed due to the heterogeneity of the outcomes.

Only findings related to anorexia nervosa (AN) were identified. Ten studies, of which seven were longitudinal, two cross-sectional, and one interventional (N = 350 patients with AN, and 304 HCs), were included. Despite no clear links between diversity metrics and clinical symptoms being observed, specific taxa belonging to phylum Firmicutes, such as Clostridium, Roseburia, Lactobacillus, Faecalibacterium, and Bifidobacterium belonging to Actinobacteriota correlated with ED psychopathology, including anxiety and depressive symptoms.

Changes in microbiota were related to anxiety and depressive symptoms, as well as altered eating behaviours by modulating inflammation and insulin pathways through short-chain fatty acids (SCFAs), that also lead to neurotransmitter imbalances. Further studies are required to replicate these finding and to explore whether similar patterns are observed in other EDs.