Celiac disease (CD) can be considered an autoimmune problem, a disease caused by gluten sensitivity in the body. Gluten is found in foods such as barley, wheat, and rye. This ailment manifests in individuals with hereditary susceptibility and under the sway of environmental stimulants, counting, in addition to gluten and intestinal microbiota dysbiosis. Currently, the only recommended treatment for this condition is to follow a gluten-free diet for life. In this review, we scrutinized the studies of recent years that focused on the use of postbiotics in vitro and in vivo in CD. The investigation of postbiotics in CD could be intriguing to observe their diverse effects on several pathways. This study highlights the definitions, characteristics, and safety issues of postbiotics and their possible biological role in the prevention and treatment of CD, as well as their application in the food and drug industry.

In recent years, the overuse of antibiotics has led to the emergence of antimicrobial-resistant (AMR) bacteria. To evaluate the spread of AMR bacteria, the reservoir of AMR genes (resistome) has been identified in environmental samples, hospital environments, and human populations, but the functional role of AMR bacteria and their persistence within individuals has not been fully investigated. Here, we performed a strain-resolved in-depth analysis of the resistome changes by reconstructing a large number of metagenome-assembled genomes from the gut microbiome of an antibiotic-treated individual. Interestingly, we identified two bacterial populations with different resistome profiles: extensively acquired antimicrobial-resistant bacteria (EARB) and sporadically acquired antimicrobial-resistant bacteria, and found that EARB showed broader drug resistance and a significant functional role in shaping individual microbiome composition after antibiotic treatment. Our findings of AMR bacteria would provide a new avenue for controlling the spread of AMR bacteria in the human community.

The increasing global incidence of precocious puberty, linked to environmental, metabolic, and genetic factors, necessitates innovative therapies beyond gonadotropin-releasing hormone (GnRH) analogs. Accumulating evidence implicates gut microbiota dysbiosis as a pivotal regulator of pubertal timing via interactions with hormone metabolism (e.g., estrogen reactivation via β-glucuronidase), neuroendocrine pathways (nitric oxide signaling), and immune-inflammatory responses. This review delineates taxonomic alterations in central precocious puberty (CPP) and obesity-related subtypes, including Streptococcus enrichment and Alistipes depletion, alongside functional shifts in microbial metabolite production. Mechanistic insights highlight microbiota-driven modulation of the hypothalamic-pituitary-gonadal (HPG) axis, leptin/insulin dynamics, and epigenetic regulation. Emerging interventions-probiotics, fecal microbiota transplantation (FMT), and dietary modifications-demonstrate efficacy in preclinical models and early clinical studies for delaying puberty onset and restoring hormonal balance. Translational efforts to validate these strategies are critical for addressing the clinical and psychosocial challenges posed by precocious puberty, positioning gut microbiota modulation as a novel therapeutic frontier in pediatric endocrinology.

The gut microbiota plays a pivotal role in human life and undergoes dynamic changes throughout the human lifespan, from infancy to old age. During our life, the gut microbiota influences health and disease across life stages. This review summarizes the discussions and presentations from the symposium "Gut microbiota development from infancy to old age" held in collaboration with the Journal of Internal Medicine. In early infancy, microbial colonization is shaped by factors such as mode of delivery, antibiotic exposure, and milk-feeding practices, laying the foundation for subsequent increased microbial diversity and maturation. Throughout childhood and adolescence, microbial maturation continues, influencing immune development and metabolic health. In adulthood, the gut microbiota reaches a relatively stable state, influenced by genetics, diet, and lifestyle. Notably, disruptions in gut microbiota composition have been implicated in various inflammatory diseases-including inflammatory bowel disease, Type 1 diabetes, and allergies. Furthermore, emerging evidence suggests a connection between gut dysbiosis and neurodegenerative disorders such as Alzheimer's disease. Understanding the role of the gut microbiota in disease pathogenesis across life stages provides insights into potential therapeutic interventions. Probiotics, prebiotics, and dietary modifications, as well as fecal microbiota transplantation, are being explored as promising strategies to promote a healthy gut microbiota and mitigate disease risks. This review focuses on the gut microbiota's role in infancy, adulthood, and aging, addressing its development, stability, and alterations linked to health and disease across these critical life stages. It outlines future research directions aimed at optimizing the gut microbiota composition to improve health.

Preterm birth is a major concern in neonatal care, significantly impacting infant survival and long-term health. The gut microbiome, essential for infant development, often becomes imbalanced in preterm infants, making it crucial to understand the effects of antibiotics on its development. Our study analyzed weekly, 6-month, and 1-year stool samples from 100 preterm infants, correlating clinical data on antibiotic use and feeding patterns. Comparing infants who received no antibiotics with those given empirical post-birth treatment, we observed notable alterations in the gut microbiome's composition and an increase in antibiotic resistance gene abundance early in life. Although these effects diminished over time, their long-term clinical impacts remain unclear. Human milk feeding was associated with beneficial microbiota like Actinobacteriota and reduced antibiotic resistance genes, underscoring its protective role. This highlights the importance of judicious antibiotic use and promoting human milk to foster a healthy gut microbiome in preterm infants.

Mammalian gut microbiomes are highly dynamic communities that shape and are shaped by host aging, including age-related changes to host immunity, metabolism, and behavior. As such, gut microbial composition may provide valuable information on host biological age. Here, we test this idea by creating a microbiome-based age predictor using 13,563 gut microbial profiles from 479 wild baboons collected over 14 years. The resulting 'microbiome clock' predicts host chronological age. Deviations from the clock's predictions are linked to some demographic and socio-environmental factors that predict baboon health and survival: animals who appear old-for-age tend to be male, sampled in the dry season (for females), and have high social status (both sexes). However, an individual's 'microbiome age' does not predict the attainment of developmental milestones or lifespan. Hence, in our host population, gut microbiome age largely reflects current, as opposed to past, social and environmental conditions, and does not predict the pace of host development or host mortality risk. We add to a growing understanding of how age is reflected in different host phenotypes and what forces modify biological age in primates.

The intestinal microbiome plays a pivotal role in maintaining host health through its involvement in gastrointestinal, immune, and central nervous system (CNS) functions. Recent evidence underscores the bidirectional communication between the microbiota, the gut, and the brain and the impact of this axis on neurological diseases, including epilepsy. In pediatric patients, alterations in gut microbiota composition-called intestinal dysbiosis-have been linked to seizure susceptibility. Preclinical models revealed that gut dysbiosis may exacerbate seizures, while microbiome-targeted therapies, including fecal microbiota transplantation, pre/pro-biotics, and ketogenic diets, show promise in reducing seizures. Focusing on clinical and preclinical studies, this review examines the role of the gut microbiota in pediatric epilepsy with the aim of exploring its implications for seizure control and management of epilepsy. We also discuss mechanisms that may underlie mutual gut-brain communication and emerging therapeutic strategies targeting the gut microbiome as a novel approach to improve outcomes in pediatric epilepsy. PLAIN LANGUAGE SUMMARY: Reciprocal communication between the brain and the gut appears to be dysfunctional in pediatric epilepsy. The composition of bacteria in the intestine -known as microbiota- and the gastrointestinal functions are altered in children with drug-resistant epilepsy and animal models of pediatric epilepsies. Microbiota-targeted interventions, such as ketogenic diets, pre-/post-biotics administration, and fecal microbiota transplantation, improve both gastrointestinal dysfunctions and seizures in pediatric epilepsy. These findings suggest that the gut and its microbiota represent potential therapeutic targets for reducing drug-resistant seizures in pediatric epilepsy.

The current discovery that the gut microbiome, which contains roughly 100 trillion microbes, affects health and disease has catalyzed a boom in multidisciplinary research efforts focused on understanding this relationship. Also, it is commonly demonstrated that the gut and the CNS are closely related in a bidirectional pathway. A balanced gut microbiome is essential for regular brain activities and emotional responses. On the other hand, the CNS regulates the majority of GI physiology. Any disruption in this bidirectional pathway led to a progression of health problems in both directions, neurological and gastrointestinal diseases. In this review, we hope to shed light on the complicated connections of the microbiome-gut-brain axis and the critical roles of gut microbiome in the early development of the brain in order to get a deeper knowledge of microbiome-mediated pathological conditions and management options through rebalancing of gut microbiome.

Monotreme and marsupial development is characterized by a short gestation, with young exposed to the environment at an early developmental stage and supported by a long lactation in the pouch, pseudo-pouch, or burrow. The lack of a functional adaptive immune system in these altricial young raises questions about how they survive in a microbe-rich environment. Previous studies on marsupial pouches have revealed changes to pouch microbe composition during lactation, but no information is available in monotremes. We investigated changes in the echidna pseudo-pouch microbiota (n = 22) during different stages of the reproductive cycle and whether this differs between wild and zoo-managed animals. Metataxonomic profiling using 16S rRNA gene sequencing revealed that pseudo-pouch microbial communities undergo dramatic changes during lactation, with significant differences in taxonomic composition compared with samples taken outside of breeding season or during courtship and mating. This suggests that the echidna pseudo-pouch environment changes during lactation to accommodate young that lack a functional adaptive immune system. Furthermore, captivity was not found to have a significant effect on pseudo-pouch microbiota. This study pioneers pouch microbiota research in monotremes, provides new biological information on echidna reproduction, and may also provide information about the effects of captive management to inform breeding programmes in the future.

The clinical efficacy of the use of probiotics, prebiotics, synbiotics and postbiotics (biotics) in cats is unknown, despite their use in daily practice. The objectives of the study is to evaluate the effectiveness of biotic supplementation in treating and preventing gastroenteropathies, and in reducing gastrointestinal signs associated with antibiotics in cats.

A systematic review was conducted by searching four databases for publications before August 2, 2024, following a pre-registered protocol. Eligible publications were trials involving healthy cats or those with gastroenteropathies, supplemented with biotics (and an inactive control), studying outcomes such as faecal consistency, faecal microbiota or vomiting. Risk of bias and quality of reports were assessed. Effects were synthesised by meta-analyses and vote counting based on direction of effect. Certainty of evidence was rated using GRADE approach.

Twenty reports were included, presenting unclear or low risk of bias. The evidence did not permit a high-confidence evaluation of the effectiveness of biotics, although five of the seven probiotic trials showed beneficial effects on faecal consistency. Synbiotics presented no clinically relevant effect in reducing antibiotics-associated vomiting, with very low certainty, in a meta-analysis including 32 adult cats. Probiotics significantly reduce the Bacillota/Actinomycetota ratio, with low certainty, in a meta-analysis involving 34 healthy young-adult cats. Following vote counting, probiotics improved immune profile in young cats, and increased butyric acid concentration in healthy cats.

Current data highlight the need for further research, especially focused on at-risk groups and sick cats, before advocating the use of biotic supplementation.

We systematically tracked early life stages in a military dog birth cohort to investigate canine gut microbiota dynamics related to environmental exposure during growth. This study utilized 16s rRNA amplicon sequencing-based analysis with molecular epidemiology of Enterococcus faecalis within a controlled environment at a military dog training center.

We examined shifts in gut microbiota diversity and taxonomic composition across four growth stages (lactation, weaning, starter, puppy) in three littermate groups. Additionally, E. faecalis dynamics was analyzed to confirm strain sharing among littermate groups.

Gut microbiota changed rapidly during early growth, stabilizing at the puppy stage. This is supported by increased similarity in taxonomic composition among littermate groups, as they experienced an increased shared external environment and consumed the identical diets. E. faecalis strain sharing among littermate groups increased as dogs aged. Nine E. faecalis cluster types were identified; three specific types (type I, II, and IX) dominated in each littermate group during lactation. With greater exposure to the shared external environment, cluster type I gradually assumed dominance across all groups. Despite the dynamic shifts in microbiota, we found five genera within the core microbiota, Bacteroides, Peptoclostridium, Fusobacterium, Lactobacillus, and Blautia.

This study is the first to explore the dynamic nature of early-life canine gut microbiota, illustrating its transition to stability and its resilience to environmental perturbations within the controlled training environment of a military dog birth cohort.

Vaccination plays a critical role in public health by reducing the incidence and prevalence of infectious diseases. The efficacy of a vaccine has numerous determinants, which include age, sex, genetics, environment, geographic location, nutritional status, maternal antibodies, and prior exposure to pathogens. However, little is known about the role of gut microbiome in vaccine efficacy and how it can be targeted through dietary interventions to improve immunological responses. Unveiling this link is imperative, particularly in the post-pandemic world, considering impaired COVID-19 vaccine response observed in dysbiotic individuals. Therefore, this article aims to comprehensively review how diet and probiotics can modulate gut microbiome composition, which is linked to vaccine efficacy. Dietary fiber and polyphenolic compounds derived from plant-based foods improve gut microbial diversity and vaccine efficacy by promoting the growth of short-chain fatty acids-producing microbes. On the other hand, animal-based foods have mixed effects - whey protein and fish oil promote gut eubiosis and vaccine efficacy. In contrast, lard and red meat have adverse effects. Studies further indicate that probiotic supplements exert varied effects, mostly strain and dosage-specific. Interlinking diet, microbiome, probiotics, and vaccines will reveal opportunities for newer research on diet-induced microbiome-manipulated precision vaccination strategies against infectious diseases.

Gut microbiome (GM) composition and function is pivotal for human health and disease, of which the virome's importance is increasingly recognised. However, prophages and their induction patterns in the infant gut remain understudied. Here, we identified 10645 putative prophages in 662 metagenomes from 1-year-old children in the COPSAC2010 mother-child cohort and investigated their potential functions. No core provirome was found as the most prevalent vOTU was identified in only ~70% of the samples. The most dominant cluster of vOTUs in the cohort was related to Bacteroides phage Hanky p00', and it carried both diversity generating retroelements and genes involved in capsular polysaccharide synthesis. Paired analysis of viromes and metagenomes from the same samples revealed that most prophages within the infant gut were induced and that induction was unaffected by a range of environmental perturbers. In summary, prophages are major components of the infant gut that may have far reaching influences on the microbiome and its host.

The development of the human immune system starts during the fetal period in a largely, but probably not completely, sterile environment. During and after birth, the immune system is exposed to an increasingly complex microbiota. The first microbiota encountered during passage through the birth canal colonize the infant gut and induce the tolerance of the immune system. Transplacentally derived maternal IgG as well as IgA from breast milk protect the infant from infections during the first 100 days, during which the immune system further develops and immunological memory is formed. The Weaning and introduction of solid food expose the immune system to novel (food) antigens and allow for other microbiota to colonize. The cells and molecules involved in the mutual and intricate interactions between microbiota and the developing immune system are now beginning to be recognized. These include bacterial components such as polysaccharide A from Bacteroides fragilis, as well as bacterial metabolites such as the short-chain fatty acid butyrate, indole-3-aldehyde, and indole-3-propionic acid. All these, and probably more, bacterial metabolites have specific immunoregulatory functions which shape the development of the human immune system during the first 1000 days of life.

Background: Vaccination constitutes a low-cost, safe, and efficient public health measure that can help prevent the spread of infectious diseases and benefit the community. The fact that vaccination effectiveness varies among populations, and that the causes of this are still unclear, indicates that several factors are involved and should be thoroughly examined. The "intestinal microbiota" is the most crucial of these elements. Numerous clinical studies demonstrate the intestinal microbiota's significance in determining the alleged "immunogenicity" and efficacy of vaccines. This systematic review aimed to review all relevant scientific literature and highlight the role of intestinal microbiota in COVID-19, Salmonella typhi, Vibrio cholerae, and rotavirus vaccinations. Materials and Methods: The MESH terms "vaccines" and "microbiota" were used to search the major scientific databases PubMed, SciVerse Scopus, Web of Knowledge, and the Cochrane Central Register of Controlled Clinical Trials. Results: Between February 2024 and October 2024, the analysis was conducted using electronic databases, yielding a total of 235 references. Finally, 24 RCTs were chosen after meeting all inclusion criteria: eight studies of COVID-19, two studies of Salmonella typhi, three studies of Vibrio cholerae, and eleven studies of rotavirus. Only six of these demonstrated good study quality with a Jadad score of three or four. Conclusions: According to the review's results, the intestinal microbiota surely plays a role in vaccinations' enhanced immunogenicity, especially in younger people. As it is still unclear what mechanisms underlie this effect, more research is needed to better understand the role of the intestinal microbiota.

Compelling evidence supports a link between early-life gut microbiota and the metabolic outcomes in later life. Using an early-life antibiotic exposure model in BALB/c mice, we investigated the life-course impact of prenatal and/or postnatal antibiotic exposures on the gut microbiome of offspring and the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Compared to prenatal antibiotic exposure alone, postnatal antibiotic exposure more profoundly affected gut microbiota development and succession, which led to aggravated endotoxemia and metabolic dysfunctions. This was primarily resulted from the overblooming of gut Parabacteroides and hepatic accumulation of cytotoxic lysophosphatidyl cholines (LPCs), which acted in conjunction with LPS derived from Parabacteroides distasonis (LPS_PA) to induce cholesterol metabolic dysregulations, endoplasmic reticulum (ER) stress and apoptosis. Integrated serum metabolomics, hepatic lipidomics and transcriptomics revealed enhanced glycerophospholipid hydrolysis and LPC production in association with the upregulation of PLA2G10, the gene controlling the expression of the group X secretory Phospholipase A2s (sPLA2-X). Taken together, our results show microbial modulations on the systemic MASLD pathogenesis and hepatocellular lipotoxicity pathways following early-life antibiotic exposure, hence help inform refined clinical practices to avoid any prolonged maternal antibiotic administration in early life and potential gut microbiota-targeted intervention strategies.

The weaning transition from a milk-based to a solid-food diet supports critical developmental changes to the intestinal microbiome and immune system. However, the specific microbial and host features that influence microbial succession at weaning are not well understood. Here, we developed a simple approach to investigate the complex dynamics of microbial succession during weaning by co-housing gnotobiotic mice colonized with the defined pre-weaning community PedsCom and the adult-derived consortium OMM12. As expected, co-housing PedsCom mice with OMM12 recapitulated microbial succession at weaning and induced immune system maturation in PedsCom mice. Unexpectedly, we found that the OMM12 microbes with the highest host glycan utilization profiles were the most adept colonizers of PedsCom mice. Genomic analysis confirmed that PedsCom is deficient in the carbohydrate-active enzymes responsible for degrading host-derived glycans, including mucins, compared to adult-derived consortia. We validated a role for glycan utilization in vivo by demonstrating that the mucus-degrading commensal microbe Akkermansia muciniphila critically depends on the metabolism of mucin glycans for colonization of PedsCom mice. These findings highlight the importance of host-derived glycans in shaping microbial communities during the weaning transition and suggest host glycans as novel targets to modulate intestinal microbial populations, introduce beneficial probiotics, and enhance immune system development during weaning.

Bacterial lipopolysaccharides (LPS) have been shown to promote enteric viral infections. This study assessed whether possessing elevated levels of LPS was associated with norovirus infection. Fecal samples from diarrheic norovirus-positive (DNP) (n = 26), non-diarrheal norovirus-negative (NDNN) (n = 26), asymptomatic norovirus-positive (ANP) (n = 15), and diarrheic norovirus-negative (DNN) (n =15) infants were assayed for selected bacterial LPS by quantitative PCR. The mean levels of selected LPS gene targets were significantly high in DNP infants (6.17 ± 2.14 CFU/g) versus NDNN infants (4.13 ± 2.25 CFU/g), p = 0.003. So too was the abundance between DNP and DNN infants (p = 0.0023). The levels of selected LPS gene targets were high regardless of whether the infection was symptomatic or asymptomatic, p = 0.3808. The average expression of genes coding for selected LPS and their signalling molecule, Toll-like receptor 4 (TLR4), increased 7- and 2.5-fold, respectively, in DNP versus NDNN children. Infants possessing elevated levels of selected LPS-rich bacteria were 1.51 times more likely to develop norovirus diarrhea (95% CI: 1.14-2.01, p = 0.004). In conclusion, norovirus infection was associated with abundance of selected bacterial LPS, suggesting a possible role of bacterial LPS in norovirus infection.

Selective antimicrobial effects have been found for α1,4-linked N-acetylglucosamine residues at the terminus of O-glycans attached to a core protein of gastric gland mucin. A4gnt encodes α1,4-N-acetylglucosaminyl transferase, which is responsible for the biosynthesis of α1,4-linked N-acetylglucosamine. The impact of A4GNT on the establishment and homeostasis of the gastric microbiome remains to be clarified. The aim of this study was to characterize the gastric microbiome in mice deficient for the production of α1,4-linked N-acetylglucosamine.

The gastric microbiome within A4gnt -/- mice and wild-type mice was analyzed using high-throughput sequencing of bacterial 16S rRNA.

In A4gnt -/- mice, which spontaneously develop gastric cancer, the community structure of the gastric microbiome was altered. The relative abundance of mutagenic Desulfovibrio and proinflammatory Prevotellamassilia in these mice was significantly increased, especially 4 weeks after birth. The co-occurrence network appeared to be much more complex. Functional prediction demonstrated considerable decreases in the relative frequencies of functions associated with polysaccharide metabolism and transportation.

The distinct profile in A4gnt -/- mice demonstrated a vital role of A4GNT in the establishment of the gastric microbiome. A dysbiotic gastric microbiome may contribute to the spontaneous development of gastric cancer in mice.

Accumulating evidence suggests that gut microbiota (GM) plays a crucial role in Alzheimer's disease (AD) pathogenesis and progression. This narrative review explores the complex interplay between GM, the immune system, and the central nervous system in AD. We discuss mechanisms through which GM dysbiosis can compromise intestinal barrier integrity, enabling pro-inflammatory molecules and metabolites to enter systemic circulation and the brain, potentially contributing to AD hallmarks. Additionally, we examine other pathophysiological mechanisms by which GM may influence AD risk, including the production of short-chain fatty acids, secondary bile acids, and tryptophan metabolites. The role of the vagus nerve in gut-brain communication is also addressed. We highlight potential therapeutic implications of targeting GM in AD, focusing on antibiotics, probiotics, prebiotics, postbiotics, phytochemicals, and fecal microbiota transplantation. While preclinical studies showed promise, clinical evidence remains limited and inconsistent. We critically assess clinical trials, emphasizing challenges in translating GM-based therapies to AD patients. The reviewed evidence underscores the need for further research to elucidate precise molecular mechanisms linking GM to AD and determine whether GM dysbiosis is a contributing factor or consequence of AD pathology. Future studies should focus on large-scale clinical trials to validate GM-based interventions' efficacy and safety in AD.

Genetic factors have been hypothesized to contribute to the heterogeneity in the response to infectious diseases (IDs). The classical twin design provides a powerful tool to estimate the role of genetic contributions to variation in infection outcomes. With this design, the impact of heritability on the proneness as well as infection- and vaccine-induced immune responses have been documented for multiple infections, including tuberculosis, malaria, leprosy, otitis media, polio, mumps, measles, rubella, influenza, hepatitis B, and human papillomavirus infections, and recently, SARS-CoV-2. The current data show the heritable aspect in nearly all infections considered. In this contribution, we review and discuss human twin studies on the heritability of host characteristics in liability and response to IDs. This review emphasizes the importance of considering factors such as sex, disease stages, and disease presentation when assessing heritability and argues that the classical twin design provides a unique circumstance for exploring the genetic contribution as twins share levels of maternal antibodies, ancestral background, often the dates and number of vaccine doses, differences in vaccines' manufacturing and storage, age, family environment, and other exposures. Additionally, we highlight the value of twin studies and the usefulness of combining the twin model with contemporary genomics technologies and advanced statistical tools to grasp a comprehensive and nuanced understanding of heritability in IDs.

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.

In the current era, malnutrition is seen as both undernutrition and overweight and obesity; both conditions are caused by nutrient deficiency or excess and improper use or imbalance in the intake of macro and micronutrients. Recent evidence suggests that malnutrition alters the intestinal microbiota, known as dysbiosis. Secretory immunoglobulin A (sIgA) plays an important role in maintaining and increasing beneficial intestinal microbiota populations and protecting against pathogenic species. Depletion of beneficial bacterial populations throughout life is also conditioned by malnutrition. This review aims to synthesize the evidence that establishes an interrelationship between diet, malnutrition, changes in the intestinal flora, and sIgA levels. Targeted nutritional therapies combined with prebiotic, probiotic, and postbiotic administration can restore the immune response in the intestine and the host's homeostasis.

Archaea have been identified as early colonizers of the human intestine, appearing from the first days of life. It is hypothesized that the origin of many of these archaea is through vertical transmission during breastfeeding. In this study, we aimed to characterize the archaeal composition in samples of mother-neonate pairs to observe the potential vertical transmission. We performed a cross-sectional study characterizing the archaeal diversity of 40 human colostrum-neonatal stool samples by next-generation sequencing of V5-V6 16S rDNA libraries. Intra- and inter-sample analyses were carried out to describe the Archaeal diversity in each sample type. Human colostrum and neonatal stools presented similar core microbiota, mainly composed of the methanogens Methanoculleus and Methanosarcina. Beta diversity and metabolic prediction results suggest homogeneity between sample types. Further, the co-occurrence network analysis showed associations between Archaea and Bacteria, which might be relevant for these organisms' presence in the human milk and neonatal stool ecosystems. According to relative abundance proportions, beta diversity, and co-occurrence analyses, the similarities found imply that there is vertical transmission of archaea through breastfeeding. Nonetheless, differential abundances between the sample types suggest other relevant sources for colonizing archaea to the neonatal gut.

Pregnancy is a transformative period marked by profound physical and emotional changes, with far-reaching consequences for both mother and child. Emerging research has illustrated the pivotal role of a mother's diet during pregnancy in influencing the prenatal gut microbiome and subsequently shaping the neurodevelopment of her offspring. The intricate interplay between maternal gut health, nutrition, and neurodevelopmental outcomes has emerged as a captivating field of investigation within developmental science. Acting as a dynamic bridge between mother and fetus, the maternal gut microbiome, directly and indirectly, impacts the offspring's neurodevelopment through diverse pathways. This comprehensive review delves into a spectrum of studies, clarifying putative mechanisms through which maternal nutrition, by modulating the gut microbiota, orchestrates the early stages of brain development. Drawing insights from animal models and human cohorts, this work underscores the profound implications of maternal gut health for neurodevelopmental trajectories and offers a glimpse into the formulation of targeted interventions able to optimize the health of both mother and offspring. The prospect of tailored dietary recommendations for expectant mothers emerges as a promising and accessible intervention to foster the growth of beneficial gut bacteria, potentially leading to enhanced cognitive outcomes and reduced risks of neurodevelopmental disorders.

Mammalian gut microbiomes are highly dynamic communities that shape and are shaped by host aging, including age-related changes to host immunity, metabolism, and behavior. As such, gut microbial composition may provide valuable information on host biological age. Here we test this idea by creating a microbiome-based age predictor using 13,563 gut microbial profiles from 479 wild baboons collected over 14 years. The resulting "microbiome clock" predicts host chronological age. Deviations from the clock's predictions are linked to some demographic and socio-environmental factors that predict baboon health and survival: animals who appear old-for-age tend to be male, sampled in the dry season (for females), and have high social status (both sexes). However, an individual's "microbiome age" does not predict the attainment of developmental milestones or lifespan. Hence, in our host population, gut microbiome age largely reflects current, as opposed to past, social and environmental conditions, and does not predict the pace of host development or host mortality risk. We add to a growing understanding of how age is reflected in different host phenotypes and what forces modify biological age in primates.

A central goal of biological anthropology is connecting environmental variation to differences in host physiology, biology, health, and evolution. The microbiome represents a valuable pathway for studying how variation in host environments impacts health outcomes. While there are many resources for learning about methods related to microbiome sample collection, laboratory analyses, and genetic sequencing, there are fewer dedicated to helping researchers navigate the dense portfolio of bioinformatics and statistical approaches for analyzing microbiome data. Those that do exist are rarely related to questions in biological anthropology and instead are often focused on human biomedicine. To address this gap, we expand on existing tutorials and provide a "road map" to aid biological anthropologists in understanding, selecting, and deploying the data analysis and visualization methods that are most appropriate for their specific research questions. Leveraging an existing dataset of fecal samples and survey data collected from wild geladas living in Simien Mountains National Park in Ethiopia (Baniel et al., 2021), this paper guides researchers toward answering three questions related to variation in the gut microbiome across host and environmental factors. By providing explanations, examples, and a reproducible workflow for different analytic methods, we move beyond the theoretical benefits of considering the microbiome within anthropological research and instead present researchers with a guide for applying microbiome science to their work. This paper makes microbiome science more accessible to biological anthropologists and paves the way for continued research into the microbiome's role in the ecology, evolution, and health of human and non-human primates.

The early life stages are critical for the development of the gut microbiome. Variables such as antibiotics exposure, birth-mode via Cesarean section, and formula feeding are associated with disruptions in microbiome development and are related to adverse health effects later in life. Studying the effects of microbiome-modulating strategies in infants is challenged by appropriate ethical constraints. Therefore, we developed I-TIM-2, an infant in vitro colonic model based on the validated, computer-controlled, dynamic model of the colon, TIM-2. The system, consisting of four separate compartments, was inoculated with feces from four healthy, primarily breastfed infants, displaying distinctive microbiome profiles. For each infant's fecal sample, a 96-h experiment was performed, with two compartments receiving an infant diet adapted medium and two compartments additionally receiving five human milk oligosaccharides (HMOs) in physiological concentrations and proportions. Bacterial composition was determined by shotgun metagenomics and qPCR. Concentrations of short-chain fatty acids (SCFAs) and HMOs were determined by LC-MS. Microbial diversity and high amounts of inoculum-derived species were preserved in the model throughout each experiment. Microbiome composition and SCFA concentrations were consistent with published data from infants. HMOs strongly modulated the microbiome composition by stimulating relative proportions of Bifidobacterium. This affected the metabolic output and resulted in an increased production of acetic and formic acid, characteristic of bifidobacterial HMO metabolism. In conclusion, these data demonstrate the development of a valid model to study the dynamics and modulations of the infant gut microbiome and metabolome.IMPORTANCEThe infant gut microbiome is intricately linked to the health of its host. This is partly mediated through the bacterial production of metabolites that interact with the host cells. Human milk shapes the establishment of the infant gut microbiome as it contains human milk sugars that select for primarily bifidobacteria. The establishment can be disrupted by modern interventions such as formula feeding. This can alter the microbiome composition and metabolite production profile, which can affect the host. In this article, we set up an infant in vitro colonic model to study microbiome interactions and functions. In this model, we investigated the effects of human milk sugars and their promotion of bifidobacteria at the expense of other bacteria. The model is an ideal system to assess the effects of various modulating strategies on the infant gut microbiome and its interactions with its host.

Radiotherapy is an effective method of treating cancer and affects 50% of patients. Intensity-modulated radiotherapy (IMRT) is a modernized method of classical radiation used in the treatment of laryngeal cancer. Treatment with intent to preserve the larynx is not always safe or complication-free. The microbiome may significantly influence the effectiveness of oncological treatment, especially radiotherapy, and may also be modified by the toxic response to radiation.

The aim of the study was to prospectively assess the microbiome and its influence on radiotherapy toxicity in patients with laryngeal cancer.

Statistically significant risk factors for complications after radiotherapy were the percentage of Porphyromonas of at least 6.7%, the percentage of Fusobacterium of at least 2.6% and the percentage of Catonella of at least 2.6%.

The importance of the microbiome in oncology has been confirmed in many studies. Effective radiotherapy treatment and the prevention of radiation-induced oral mucositis is a challenge in oncology. The microbiome may be an important part of personalized cancer treatment. The assessment of the microbiome of patients diagnosed with cancer may provide the opportunity to predict the response to treatment and its effectiveness. The influence of the microbiome may be important in predicting the risk group for radiotherapy treatment failure. The possibility of modifying the microbiome may become a goal to improve the prognosis of patients with laryngeal cancer. Fusobacterium, Porphyromonas and Catonella are important risk factors for radiation-induced oral mucositis in patients with laryngeal cancer.

Recent studies have shown that 1-oleo-2-palmito-3-linoleyl glycerol (OPL) is the most abundant triacylglycerol in human breast milk in China. Epidemiologic studies have shown that sn-2 palmitate improves the absorption of fatty acids and calcium in infants. However, there have been few studies of the specific mechanism by which OPL affects intestinal function. In the present study, we have characterized the effects of various levels of OPL supplementation on the development of the intestinal epithelium and the intestinal microbiota of neonatal mice. OPL supplementation increased the body masses and intestinal lengths of weaned mice and promoted defecation. These positive effects were related to the effect of OPL to promote the development of intestinal villi and crypts. OPL increased the expression of the intestinal stem cell markers Olfm4 and Sox9 in the jejunum and ileum, which promoted their differentiation into goblet cells and Paneth cells. It also promoted the integrity of the epithelial barrier by increasing the secretion of mucin 2 and lysozyme 1 and the expression of the tight junction proteins occludin, ZO1, claudin 2, and claudin 3. More importantly, we found that low dose-OPL promotes the transformation of the intestinal microbiota of neonatal mice to the mature state in 3-month-old mice, increases the proportion of Firmicutes, and reduces the proportion of Bacteroidota. The proportions of anaerobic genera of bacteria, such as Lachnospiraceae_NK4A136_group, Lachnoclostridium, Ligilactobacillus, and Bifidobacterium were higher, as were the key producers of short-chain fatty acids, such as Bacteroides and Blautia. OPL also increased the butyric acid content of the feces, which significantly correlated with the abundance of Lactobacillus. High-dose OPL tended to be more effective at promoting defecation and the development of the villi and crypts, but these effects did not significantly differ from those achieved using the lower dose. A low dose of OPL was more effective at increasing the butyric acid content and causing the maturation of microbes. In summary, the OPL supplementation of newborn mice promotes the establishment of the intestinal epithelial layer structure and barrier function, and also promotes the transformation of the intestinal microbiota to a mature state. This study lays a theoretical foundation for the inclusion of OPL in infant formula and provides a scientific basis for the development of intestinal health products.

Antimicrobial resistance is an urgent threat to human health. Asymptomatic colonization is often critical for persistence of antimicrobial-resistant pathogens. Gut colonization by the antimicrobial-resistant priority pathogen Acinetobacter baumannii is associated with increased risk of clinical infection. Ecological factors shaping A. baumannii gut colonization remain unclear. Here we show that A. baumannii and other pathogenic Acinetobacter evolved to utilize the amino acid ornithine, a non-preferred carbon source. A. baumannii utilizes ornithine to compete with the resident microbiota and persist in the gut in mice. Supplemental dietary ornithine promotes long-term fecal shedding of A. baumannii. By contrast, supplementation of a preferred carbon source-monosodium glutamate (MSG)-abolishes the requirement for A. baumannii ornithine catabolism. Additionally, we report evidence for diet promoting A. baumannii gut carriage in humans. Together, these results highlight that evolution of ornithine catabolism allows A. baumannii to compete with the microbiota in the gut, a reservoir for pathogen spread.

Introduction: Head and neck squamous cell carcinoma (HNSCC) ranks sixth among cancers in the world, and the 5-year survival rate ranges from 25% to 60%. The risk factors for HNSCC are primarily smoking, alcohol consumption and human papillomavirus (HPV). Data indicate that 15-20% of cancers are caused by infectious agents, 20-30% by smoking and 30-35% by unhealthy lifestyles, diet, lack of physical activity and obesity. Dysbiosis is a microbiome imbalance, which promotes oncogenesis by intensifying inflammatory processes and affecting the host's metabolism. Profiling the microbiome in various types of cancer is currently the subject of research and analysis. However, there is still little information on the correlation of the microbiome with HNSCC and its impact on oncogenesis, the course of the disease and its treatment. Objective: The aim of the study was to prospectively assess risk factors with assessment of the impact of the microbiome on the risk of squamous cell carcinoma of the larynx. The study included a group of 44 patients diagnosed with squamous cell carcinoma of the larynx and 30 patients from the control group. Results: In the control group, bacteria of the normal microbiome dominated-the genus Streptococcus, Gemella, Neisseria and Kingella. In the group of patients with laryngeal cancer, Prevotella, Clostridiales and Stomatobaculum were found significantly more often. Porphyromonas, Fusobacterium, Lactobacillus, Actinobacteria, Actinomyces and Shaalia odontolytica were also found at a higher percentage in the study group. Analyzing the phylum, Firmicutes dominated in the control group; there were statistically significantly more of them than in patients from the study group. Bacteroides and Bacillota were found significantly more often in patients with laryngeal cancer. Conclusions: The importance of the microbiome in oncology has been confirmed in many studies. Independent risk factors for laryngeal cancer were primarily a lower number of Firmicutes in the microbiome, but also an increased leukocyte level above 6.52 × 103/mm and a decreased total protein level below 6.9 g/dL. Prevotella, Clostridiales, Stomatobaculum, Porphyromonas, Fusobacterium, Lactobacillus, Actinobacteria, Actinomyces and Shaalia were considered to be the bacteria contributing to the development of laryngeal cancer. Streptococcus, Gemella, Neisserie and Kingella were considered to be protective bacteria. Moreover, the study confirmed the significant impact of smoking, alcohol consumption and poor oral hygiene on the development of laryngeal cancer. The microbiome, its identification and manipulation may constitute a breakthrough discovery for improving the diagnosis and oncological therapy of laryngeal cancer, and also of the entire group of HNSCC. Profiling the microbiome may allow for personalized therapy related to its modification. Assessing the microbiome of patients diagnosed with cancer may provide an opportunity to predict treatment response and effectiveness.

Stunting can be linked to various factors, one of which is dysbiosis. This study aims to analyze the microbiota composition and related contributing factors of stunted and non-stunted children in the slum areas of Jakarta.

The subjects in this study included 21 stunted (HAZ ≤ -2SD) and 21 non-stunted children (-2SD ≤ HAZ ≤ 3SD) aged 2-5 years. Microbiota analysis was performed by extracting DNA from the subjects' feces and then via 16S rRNA sequencing using next-generation sequencing (NGS).

The results of this study showed that in stunted children, the abundance of Mitsuokella (24,469 OTUs), Alloprevotella (23,952 OTUs), and Providencia alcalifaciens (861 OTUs) was higher, while in non-stunted children, that of Blautia (29,755 OTUs), Lachnospiraceae (6134 OTUs), Bilophila (12,417 OTUs), Monoglobus (484 OTUs), Akkermansia muciniphila (1116 OTUs), Odoribacter splanchnicus (42,993 OTUs), and Bacteroides clarus (8900 OTUs) was higher. Differences in microbiota composition in the two groups were influenced by nutrient intake, birth history, breastfeeding history, handwashing habits before eating, drinking water sources, and water sources for other activities.

This study highlights that stunted children have a significantly different gut microbiota composition compared to non-stunted children, with higher levels of pathogenic bacteria and lower levels of beneficial bacteria. Future research should focus on interventions that can improve the gut microbiota composition to prevent stunting in children.

Premature infants, defined as those born before 37 weeks of gestation, face numerous health challenges due to their underdeveloped systems. One critical aspect of their health is the gut microbiota, which plays a vital role in their immune function and overall development. This study provides a comprehensive bibliometric analysis of research trends, influential contributors, and evolving themes in the study of gut microbiota in premature infants over the past two decades.

We conducted a bibliometric analysis using the Web of Science Core Collection database, covering publications from January 1, 2004, to June 17, 2024. We employed VOSviewer, the R package "bibliometrix", and Citespace for data visualization and analysis, focusing on co-authorship, co-citation, and keyword co-occurrence networks.

The temporal analysis revealed a significant increase in research output on gut microbiota in premature infants, particularly in the last decade. Early research primarily focused on characterizing the gut microbiota of premature infants, identifying less diversity and a higher prevalence of pathogenic bacteria compared to full-term infants. Key research themes identified include probiotics, necrotizing enterocolitis (NEC), and breastfeeding. Probiotic studies highlighted the potential of strains like Bifidobacterium and Lactobacillus in reducing NEC and sepsis incidences. Breastfeeding research consistently showed the benefits of human milk in fostering a healthier gut microbiota profile. Co-authorship and co-citation analyses identified key contributors and influential studies, emphasizing strong international collaborations, particularly among researchers from the United States, China, and European countries.

This bibliometric analysis underscores the growing recognition of the gut microbiota's crucial role in the health of premature infants. The field has seen significant advancements, particularly in understanding how interventions like probiotics and breastfeeding can modulate gut microbiota to improve health outcomes. Continued research and international collaboration are essential to further unravel the complexities of gut microbiota in premature infants and develop effective therapeutic strategies.

Understanding the colonization and change patterns of gut microbiota is pivotal for comprehending host health. As a newly cultured breed, the studies on the gut microbiota of Tianfu goats remain limited. This study aimed to address this gap by analyzing the microbial composition and colonization patterns of fecal samples collected from goat kids from birth to weaning. Fecal samples were collected on days 0, 7, 14, 21, 28, 35, 42, 49, 53, 55, 57, and 64, and the changes and colonization patterns of microorganisms were analyzed through high-throughput 16S rRNA sequencing. The results showed that the abundance of fecal microbiota in goat kids gradually increased over time, followed by a decrease after weaning and stabilization, with reduced individual differences. The colonization of fecal microorganisms mainly presented three different stages: days 0-14, days 21-49, and days 53-64. During the suckling period, the relative abundance of Proteobacteria (72.34%) was the highest, followed by Firmicutes (21.66%). From 21 days old, the microbiota in goat kids gradually to be diverse, with Lachnospiraceae and Ruminococcaceae being dominant. During post-weaning, Ruminococcaceae (30.98-33.34%) was becoming prominence which helpful for cellulose decomposition. LEfSe analyzed three important time points (d0 vs. d7, d7 vs. d14, d49 vs. d53, LDA score > 4 and p < 0.05), 53 microbial communities with stage differences were identified. Functional prediction using PICRUSt revealed that differential microbial communities are mainly related to carbohydrate and amino acid metabolism pathways. Overall, this study addresses the intricate relationship between ages, diets, and microbiota compositions in Tianfu goat kids, and also offering insights into microorganisms-host interactions.

Sepsis is a severe disease that occurs when the body's immune system reacts excessively to infection. The body's response, which includes an intense antibacterial reaction, can damage its tissues and organs. Neutrophils are the major components of white blood cells in circulation, play a vital role in innate immunity while fighting against infections, and are considered a feature determining sepsis classification. There is a plethora of basic research detailing neutrophil functioning, among which, the study of neutrophil extracellular traps is providing novel insights into mechanisms and treatments of sepsis. This review explores their functions, dysfunctions, and influences in the context of sepsis. The interplay between neutrophils and the human microbiome and the impact of DNA methylation on neutrophil function in sepsis are crucial areas of study. The interaction between neutrophils and the human microbiome is complex, particularly in the context of sepsis, where dysbiosis may occur. We highlight the importance of deciphering neutrophils' functional alterations and their epigenetic features in sepsis because it is critical for defining sepsis endotypes and opening up the possibility for novel diagnostic methods and therapy. Specifically, epigenetic signatures are pivotal since they will provide a novel implication for a sepsis diagnostic method when used in combination with the cell-free DNA. Research is exploring how specific patterns of DNA methylation in neutrophils, detectable in cell-free DNA, could serve as biomarkers for the early detection of sepsis.

Methanobrevibacter smithii (M. smithii), initially isolated from human feces, has been recognised as a distinct taxon within the Archaea domain following comprehensive phenotypic, genetic, and genomic analyses confirming its uniqueness among methanogens. Its diversity, encompassing 15 genotypes, mirrors that of biotic and host-associated ecosystems in which M. smithii plays a crucial role in detoxifying hydrogen from bacterial fermentations, converting it into mechanically expelled gaseous methane. In microbiota in contact with host epithelial mucosae, M. smithii centres metabolism-driven microbial networks with Bacteroides, Prevotella, Ruminococcus, Veillonella, Enterococcus, Escherichia, Enterobacter, Klebsiella, whereas symbiotic association with the nanoarchaea Candidatus Nanopusillus phoceensis determines small and large cell variants of M. smithii. The former translocate with bacteria to induce detectable inflammatory and serological responses and are co-cultured from blood, urine, and tissular abscesses with bacteria, prototyping M. smithii as a model organism for pathogenicity by association. The sources, mechanisms and dynamics of in utero and lifespan M. smithii acquisition, its diversity, and its susceptibility to molecules of environmental, veterinary, and medical interest still have to be deeply investigated, as only four strains of M. smithii are available in microbial collections, despite the pivotal role this neglected microorganism plays in microbiota physiology and pathologies.

Breastfeeding and microbial colonization during infancy occur within a critical time window for development, and both are thought to influence the risk of respiratory illness. However, the mechanisms underlying the protective effects of breastfeeding and the regulation of microbial colonization are poorly understood. Here, we profiled the nasal and gut microbiomes, breastfeeding characteristics, and maternal milk composition of 2,227 children from the CHILD Cohort Study. We identified robust colonization patterns that, together with milk components, predict preschool asthma and mediate the protective effects of breastfeeding. We found that early cessation of breastfeeding (before 3 months) leads to the premature acquisition of microbial species and functions, including Ruminococcus gnavus and tryptophan biosynthesis, which were previously linked to immune modulation and asthma. Conversely, longer exclusive breastfeeding supports a paced microbial development, protecting against asthma. These findings underscore the importance of extended breastfeeding for respiratory health and highlight potential microbial targets for intervention.