Diabetes Mellitus, characterized by insufficient insulin secretion, pancreatic beta cell damage, or insulin resistance, is the third most prevalent chronic metabolic disease worldwide. Polysaccharides, biocompatible natural macromolecules, have garnered significant attention for their potential in modulating diabetes through various mechanisms. Despite extensive studies, a comprehensive and impartial evaluation of anti-diabetic polysaccharides (ATDPs) research is still lacking. This study employs bibliometric and knowledge mapping techniques to analyze research trends and developments concerning ATDPs. A total of 3435 publications from 2001 to 2024 were examined, revealing a marked increase in publication volume and citation frequency, particularly since 2016. Network analysis indicates China as the leading contributor, with the highest number of publications and prominent institutions. The International Journal of Biological Macromolecules is identified as the most prolific journal in this field. Shaoping Nie stands out as a leading researcher with the highest citation frequency and h-index. Current research trends focus on the role of polysaccharides in regulating oxidative stress and inflammation, modulation of gut microbiota, and their structural characterization. Emerging studies investigate how these polysaccharides impact gut microbiota composition, enhance intestinal barrier functions, and modulate immune responses, representing cutting-edge areas in diabetes research. This research pioneers the use of bibliometric analysis to map ATDPs research trajectories, offering valuable insights into prevailing trends, emerging topics, and opportunities for future research and collaboration.

Weightlessness usually causes disruption of the gut microbiota and impairs cognitive function. There is a close connection between gut microbiota and neurological diseases. Low-intensity pulsed ultrasound (LIPUS) has a beneficial effect on reducing intestinal inflammation. So we wondered if abdominal LIPUS stimulation can have a positive impact on weightlessness induced cognitive decline by reducing intestinal dysfunction. The findings revealed that the hind limb unloaded mice exhibited evident disruption in intestinal structure and gut microbial homeostasis, along with impairment in their learning and memory capabilities. However, 4-week abdominal LIPUS treatment improved intestinal function in hind limb unloaded mice, characterized by upregulation of tight junction proteins ZO-1 and Occludin expression in the colon, increased diversity and abundance of intestinal microbiota, decreased serum lipopolysaccharide (LPS), and increased short chain fatty acids in colon contents. The hind limb unloaded mice treated with LIPUS exhibited heightened activity levels, improved exploratory tendencies, and significantly enhanced learning and memory faculties, and elevated expression of neuroadaptation-related proteins such as PSD95, GAP43, P-CREB, BDNF, and its receptor TRKB in the hippocampus. Furthermore, the hind limb unloaded mice receiving fecal transplants from the mice whose abdomens were irradiated with LIPUS displayed enhanced cognitive abilities and improved intestinal structure, akin to the outcomes observed in hind limb unloaded mice who received LIPUS abdominal treatment directly. The above results indicate that LIPUS enhances intestinal structure and microbiota, which helps alleviate cognitive impairment caused by weightlessness. LIPUS could be a potential strategy to simultaneously improve gut dysfunction and cognitive decline in astronauts or bedridden patients.

Microbial infections have been a widely studied area of disease research since historical times, yet they are a cause of severe illness and deaths worldwide. Furthermore, infections by pathogens are not just restricted to humans; instead, a diverse range of hosts, including plants, livestock, marine organisms and fish, cause significant economic losses and pose threats to humans through their transmission in the food chain. It is now believed that both the pathogen and the host contribute to the outcomes of a disease pathology. Researchers have unravelled numerous aspects of host-pathogen interactions, offering valuable insights into the physiological, cellular and molecular processes and factors that contribute to the development of infectious diseases. Polyamines are key factors regulating cellular processes and human ageing and health. However, they are often overlooked in the context of host-pathogen interactions despite playing a dynamic role as a defence molecule from the perspective of the host as well as the pathogen. They form a complex network interacting with several molecules within the cell, with reactive oxygen species being a key component. This review presents a thorough overview of the current knowledge of polyamines and their intricate interactions with reactive oxygen species in the infection of multiple pathogens in diverse hosts. Interestingly, the review covers the interplay of the commensals and pathogen infection involving polyamines and reactive oxygen species, highlighting an unexplored area within this field. From a future perspective, the dynamic interplay of polyamines and oxidative stress in microbial pathogenesis is a fascinating area that widens the scope of developing therapeutic strategies to combat deadly infections.

Ecological niches present unique environmental and biological trademarks such as abiotic conditions, nutrient availability, and trophic interactions that may impact the ecology of living organisms. Female mosquitoes deposit their eggs in aquatic niches with fluctuating diet sources and microbial communities. However, how niche's diet and microbial composition impact mosquito performance (i.e., traits that maximize mosquito fitness) are not well understood. In this study, we focused on the Asian tiger mosquito, Aedes albopictus, one of the most invasive species in the world and a competent vector for human pathogens. To remove any external microbes, Ae. albopictus eggs were surface-sterilized then hatching larvae were exposed to a gradient of bacterial inoculum (i.e., initial microbial load) and diet concentrations while their impact on mosquito performance traits during juvenile development was measured.

Our results showed that Ae. albopictus larvae develop faster and give larger adults when exposed to microbiota in rearing water. However, mosquito performance, up to the adult stage, depends on both bacterial inoculum size and diet concentration in the aquatic habitat. Upon low inoculum size, larvae survived better if the diet was in sufficient amounts whereas a higher inoculum size was associated with optimal larvae survival only in the presence of the lower amount of diet. Inoculum size, and to a lesser extent diet concentration, shaped bacterial community structure and composition of larval-rearing water allowing the identification of bacterial taxa for which their abundance in larvae-rearing water correlated with niche parameters and/or larval traits.

Our work demonstrates that both diet concentration and bacterial inoculum size impact mosquito performance possibly by shaping bacterial community structure in the larval habitat, which accounts for a large part of the juvenile's microbiota. Host-microbe interactions influence several mosquito life-history traits, and our work reveals that niche parameters such as inoculum size and diet concentration could have numerous implications on the microbiota assembly and host evolutionary trajectory. This underlies that host-microbe-environment interactions are an important yet overlooked factor of mosquito adaptation to its local environment, with potential future implications for vector control and vector ecology. Video Abstract.

The gut microbiota constitutes a complex ecosystem essential for host health, offering metabolic support, modulating the immune system, and protecting against pathogens. However, this community faces constant destabilizing challenges, including dietary changes, antibiotics, and enteric infection. Prolonged microbiota imbalance or dysbiosis can exacerbate intestinal disease states, including inflammatory bowel disease and colorectal cancer. Understanding the mechanisms that sustain microbiota resilience in the face of these imbalances is crucial for maintaining host health and developing effective therapeutics. This review explores microbiota resilience through the lens of an ecological model, emphasizing the interplay between microbial communities and host-driven environmental controls. We highlight two critical factors shaping microbiota resilience: oxygen tension and iron availability-challenges encountered by ancient anaerobic organisms during early evolutionary history, from which the predominant members of the microbiota have descended. Disruptions in intestinal anaerobiosis during inflammation increase luminal oxygen levels, favoring pro-inflammatory facultative anaerobes and depleting obligately anaerobic commensals. Simultaneously, host nutritional immunity restricts iron availability, further challenging commensal survival. This dual environmental challenge of rising oxygen tension and reduced iron availability is a convergent outcome of a diverse array of perturbations, from pathogen invasion to antibiotic treatment. By highlighting these conserved downstream environmental challenges rather than the specific upstream perturbations, this ecological view offers a focused framework for understanding microbiota resilience. This perspective not only enhances our understanding of host-microbiota interactions but also informs therapeutic strategies to foster resilience and support host health.

Elucidating the specific processes and drivers of community assembly in the host microbiome is essential to fully understand host biology. Toward this goal, an important first step is to describe co-occurrence patterns among different microbial taxa, which can be driven by numerous factors, such as host identity. While host identity can be an important influential factor on co-occurrence patterns, a limited number of studies have explored the relative importance of host identity after controlling for other environmental factors. Here, we examined microbial co-occurrence patterns in four phylogenetically distinct trematode species living within the same snail species, collected concomitantly from the same habitat. Our previous study determined that all these trematodes shared some bacterial taxa, and the relative abundance of microbial taxa differed among trematodes, possibly due to differences in their eco-physiological traits. Here, we specifically predict that pairwise microbial co-occurrence patterns also vary among trematode host species. Our results showed that co-occurrence patterns among eight microbial families varied greatly among the four trematode hosts, with some microbial families co-occurring in some trematode species, whereas no such patterns were observed in other trematodes. Our study suggests that the habitat identity (trematode species) and its associated biotic characteristics, such as physiological and ecological traits, can determine co-occurrence patterns among microbial taxa, with substantial effects on local community composition.

Acute lymphoblastic leukemia (ALL) stands out as the most prevalent neoplasm during childhood, characterized by the rapid production of abnormal lymphoid cells. Chemotherapy administered to these patients may induce a substantial imbalance in the oral microbiota. A prospective pediatric study encompassing a control group (without ALL) and ALL patients at two treatment stages (pre-induction and consolidation) was conducted. Clinical and laboratory data were meticulously collected. Moreover, DNA from saliva samples was extracted for 16S rRNA sequencing. Clinical data revealed a heightened incidence of oral mucositis during the consolidation phase. Analysis of alpha biodiversity (observed taxa) exhibited a significant reduction in bacterial richness among patients in the consolidation phase. Network analysis identified key taxa during this phase, namely Neisseria flavescens, Prevotella melaninogenica and Porphyromonas. The findings underscore the substantial impact of ALL treatment on the oral microbiota composition, indicating diminished bacterial diversity and an elevated prevalence of oral mucositis.

Human health is influenced by the gut microbiota, particularly in aspects of host immune homeostasis and intestinal immune response. Tryptophan (Trp) not only acts as a nutrient enhancer but also plays a critical role in the balance between host immune tolerance and gut microbiota maintenance. Both endogenous and bacterial metabolites of Trp, exert significant effects on gut microbial composition, microbial metabolism, the host immunity and the host-microbiome interface. Trp metabolites regulate host immunity by activating aryl hydrocarbon receptor (AhR), thereby contributing to immune homeostasis. Among Trp metabolites, AhR ligands include endogenous metabolites (such as kynurenine), and bacterial metabolites (such as indole and its derivatives). Here, we present a comprehensive analysis of the relationships between Trp metabolism and 14 key microbiota, encompassing fungi (e.g., Candida albicans, Aspergillus), bacteria (e.g., Ruminococcus gnavus, Bacteroides, Prevotella copri, Clostridium difficile, Escherichia coli, lactobacilli, Mycobacterium tuberculosis, Pseudomonas aeruginosa, Staphylococcus aureus, Helicobacter. Pylori), and viruses (e.g., SARS-CoV-2, influenza virus). This review clarifies how the gut microbiota regulates Trp metabolism and uncovers the underlying mechanisms of these interactions. And increased mechanistic insight into how the microbiota modulate the host immune system through Trp metabolism may allow for the identification of innovative therapies that are specifically designed to target Trp absorption, Trp metabolites, the gut microbiota, or interactions between Trp and gut microbiota to treat both intestinal and extra-intestinal inflammation as well as microbial infections.

Mice are colonized by diverse gut fungi, known as the mycobiota, which have received much less attention than bacterial microbiota. Here, we studied the diversities and structures of cecal fungal communities in wild (Lasiopodomys brandtii, Apodemus agrarius, and Microtus fortis) vs laboratory C57BL/6J mice to disentangle the contributions of gut fungi to the adaptation of mice to genetic diversity. Using ITS1 gene sequencing, we obtained 2,912 amplicon sequence variants (ASVs) and characterized the composition and diversity of cecal mycobiota in mice. There were significant differences in the composition of cecal fungal communities between wild and C57BL/6J mice, with more species diversity and richness of fungi in wild mice than C57BL/6J mice. We cultured 428 fungal strains from the cecal mycobiota, sequenced the whole genome of 48 selected strains, and identified 500,849 genes. Functional annotation analysis revealed multiple pathways related to energy metabolism, carbohydrate metabolism, fatty acid metabolism, and enzymes involved in the degradation of polysaccharides, lipids, and proteins, and secondary metabolite biosynthesis. The functions and abundance of Hypocreales and Pleosporales, which included the majority of the crucial metabolic pathways, were significantly higher in wild mice than in C57BL/6J mice. The results suggest that variations in the fungal community composition may relate to the adaptability of mice to their environmental habitats.

In this study, we analyzed the fungal microbiota of three wild mouse species alongside laboratory mice using ITS1 amplicon sequencing. By integrating whole-genome sequencing with culturomics, we sequenced the genomes of 48 fungi isolated from cultured strains and investigated their biological functions to understand the role of intestinal fungi in the environmental adaptability of wild mice. This investigation has expanded the functional gene repository of gut fungi and shed new light on the intricate interplay between mice and their gut fungal communities. The data offer valuable insight into the ecological adaptation in wild mice, emphasizing the complex and dynamic relationship between the murine hosts and their mycobiota.

Anorexia nervosa (AN) is a complex psychiatric disorder characterized by persistent dieting and reduced food intake, leading to significantly low body weight. Dysbiosis in the gut microbiome of patients with AN has been suggested to contribute to the pathogenesis. Here, we used fecal microbiota transplantation (FMT) in the activity-based anorexia (ABA) rat model to investigate the impact of AN-associated gut microbiota on disease-related outcomes.

We validated the FMT in 12 Wistar rats by depleting the gut microbiome with antibiotics and transplanting two donors' fecal samples. We then transplanted fecal samples from four patients with AN or four healthy controls in 48 rats just before the ABA model exposure and included an antibiotic-only control group. During ABA, the rats had access to a running wheel and only 1.5 h access to chow for 7 days. We monitored body weight, body temperature, food intake, wheel revolutions, and gut microbiome biodiversity and composition.

The antibiotic treatment significantly depleted the rats' gut microbiome and subsequent transplantation made the rats' microbiome more similar to the donors' microbiome. The antibiotic-only group showed reduced survival, as well as lower body weight and temperature during ABA. Transplanted microbiota from patients with AN and healthy controls improved outcomes in the ABA model.

We do not find evidence that the microbiome of patients with AN differentially contributes to anorexia-like phenotypes based upon partial microbiome transplantation. However, the presence of a microbiome impacts the outcome of the ABA model.

As coral diseases become more prevalent and frequent, the need for new intervention strategies also increases to counteract the rapid spread of disease. Recent advances in coral disease mitigation have resulted in increased use of antibiotics on reefs, as their application may halt disease lesion progression. Although efficacious, consequences of deliberate microbiome manipulation resulting from antibiotic administration are less well-understood- especially in non-diseased corals that appear visually healthy. Therefore, to understand how apparently healthy corals are affected by antibiotics, we investigated how three individual antibiotics, and a mixture of the three, impact the microbiome structure and diversity of a disease-resistant Caribbean staghorn coral (Acropora cervicornis) genotype. Over a 96-hour, aquarium-based antibiotic exposure experiment, we collected and processed coral tissue and water samples for 16S rRNA gene analysis.

We found that antibiotic type and dose distinctively impact microbiome alpha diversity, beta diversity, and community composition. In experimental controls, microbiome composition was dominated by an unclassified bacterial taxon from the order Campylobacterales, while each antibiotic treatment significantly reduced the relative abundance of this taxon. Those taxa that persisted following antibiotic treatment largely differed by antibiotic type and dose, thereby indicating that antibiotic treatment may result in varying potential for opportunist establishment.

Together, these data suggest that antibiotics induce microbiome dysbiosis- hallmarked by the loss of a dominant bacterium and the increase in taxa associated with coral stress responses. Understanding the off-target consequences of antibiotic administration is critical not only for informed, long-term coral restoration practices, but also for highlighting the importance of responsible antibiotic dissemination into natural environments.

Exposure to chemical pollutants and their effects on the gut microbiome during early life are scarce, especially the effects of mixed exposures. Plasma pollutants levels were measured using gas chromatography -triple quadrupole mass spectrometer (GC-MS/MS) among 304 infants in the neonatal ward at Hunan Children's hospital, China, and gut microbiota was derived from 16S rRNA sequencing. We assessed exposure and alpha diversity using generalized linear models, and variation in beta diversity (Bray-Curtis), taxa abundance (MaAsLin2), and employed Bayesian kernel machine regression (BKMR) to investigate the association of pollutants mixture with alpha diversity and taxa. PBDE-99 was positively associated with the Chao1 index (β = 4.29, 95%CI:1.54,7.03). Exposure to the pesticides trifluralin, γ-BHC, and methidathion significantly affected beta diversity (all PFDR < 0.05). PBDE-100, β-BHC, phosalone, methiamitron, fenpropathrin, δ-BHC, and o,p'-DDT were associated with changes in taxa abundance, including negative associations [e.g., Staphylococcus, Bacteroides, Bifidobacterium, and Corynebacterium] and positive associations [e.g., Acinetobacter and Pseudomonas]. An interaction between o,p'-DDT and δ-BHC on Pseudomonas was also found in BKMR models. Our findings suggest that chemical pollutants are associated with gut microbiome changes in hospitalized infants, providing new insights into the mechanisms of chemical pollutants toxicity. Further validation is necessary to confirm these associations and explore their long-term health effects.

Bee pollen, a natural honeybee product, is hailed as a treasure trove of human nutrition. Among the nourishing substances of bee pollen, the constituents with a low molecular weight (such as phenolic acids and flavonoid glycosides) have been extensively studied in the past decades, whereas the polysaccharides with a relatively high molecular weight have received much less attention. To deepen our understanding of bee pollen polysaccharides, this review summarizes the published findings related to their preparation technologies, structural characteristics and biological activities. Among the preparation technologies, ultrasonic-assisted extraction is currently the most effective technology for the recovery of polysaccharides from bee pollen, because ultrasound can crack the pollen exine into fragments and facilitate the release of polysaccharides present in the pollen intine. The preliminary structures, including the molecular weight and monosaccharide composition, of bee pollen polysaccharides have been widely reported, but their fine structures have not fully elucidated. Moreover, bee pollen polysaccharides have antioxidant, immunomodulatory, and antitumor activities, exhibiting potential application in functional foods. Furthermore, bee pollen polysaccharides can modulate the composition of gut microbiota and promote the production of short-chain fatty acids. It is expected that this review can provide inspiration for the development and utilization of bee pollen polysaccharides.

This study aimed to investigate the effects of Boletus edulis Bull: Fr. polysaccharide (BEP), extracted using a deep eutectic solvent based on l-lactic acid and glycine, on glucose and lipid metabolism in high-fat diet (HFD)-fed mice. The primary mechanism by which BEP improves symptoms of glucose and lipid imbalances involves the modulation of gut microbiota. Key beneficial bacteria, including S24-7, Lachnospiraceae, [Prevotella], and Lactobacillus, were significantly enriched in the intestines of BEP-treated mice, with abundances 2.48-, 1.62-, 6.33- and 2.60-fold higher, respectively, compared to the HFD group. In contrast, the abundance of harmful bacteria, particularly Desulfovibrio, was reduced by 1.81-fold. These microbial shifts contributed to the alleviation of intestinal mucus layer damage and a 50 % reduction in serum lipopolysaccharide (LPS) levels, a key driver of systemic inflammation, compared to the HFD group. As a result, BEP effectively inhibited LPS-induced activation of the hepatic TLR4/Myd88/MAPK signaling pathway, thereby normalizing the expression of proteins related to glucose and lipid metabolism. A fecal microbiota transplantation study further demonstrated that the gut microbiota changes induced by BEP were central to its anti-metabolic syndrome effects. Overall, BEP may serve as a dietary supplement for preventing and treating diet-induced metabolism disorders by targeting the gut microbiota.

The prevalence of neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, is steadily increasing, thus posing significant challenges to global healthcare systems. Emerging evidence suggests that dietary habits, particularly consumption of high-fat diets, may play a pivotal role in the development and progression of neurodegenerative disorders. Moreover, several studies have shed light on the intricate communication between the gut and the brain, linking gut health with neuroinflammation and its involvement in neurodegenerative processes. This study aims to assess the effects of a high-fat dietary intake on various aspects of neuronal function during aging in a gender specific manner to help understand the potential contributions of diet to neuronal function. To investigate the effects of a high-fat diet, Drosophila melanogaster was used and exposed to a standard normal food diet (NF) and a high-fat diet (HF). Adults were grouped at 10 and 45 days of age in male and female flies reared under the same conditions starting the HF diet at 5 days of age with data showing differential gender- and HF diet-induced phenotypes. Malondialdehyde (MDA) levels were higher in males at 10 and 45 days (p < 0.05), caspase-3 expression increased at 45 days (p < 0.01) implicating apoptosis induction and a reduced climbing activity at 10 and 45 days was apparent in females only (p < 0.01). Adult lifespan under both dietary conditions was unchanged when reared at 18°C but odour-associated learning ability was reduced in larvae reared in a HF diet throughout their development (p < 0.05). This is the first study to characterise effects of a HF diet on neuronal phenotypes in an age- and gender-specific manner in a Drosophila model. Our findings suggest a HF diet induces differential effects of neuronal dysfunction with age and sex-specific outcomes, characterised by enhanced oxidative stress and cell death impacting on behaviour.

Lactobacillaceae are a large, diverse family of Gram-positive lactic acid-producing bacteria. As gut microbiota residents in many mammals, these bacteria are beneficial for health and frequently used as probiotics. Lactobacillaceae abundance in the gastrointestinal tract has been correlated with gastrointestinal pathologies and infection. Microbiota residents must compete for nutrients, including essential metal ions like calcium, zinc, and iron. Recent animal and human studies have revealed that dietary calcium can positively influence the diversity of the gut microbiota and abundance of intestinal Lactobacillaceae species, but the underlying molecular mechanisms remain poorly understood. Here, we investigated the impacts of calcium on the growth and biofilm formation of two distinct Lactobacillaceae species found in the gut microbiota, Lactobacillus acidophilus ATCC 4356 and Lactiplantibacillus plantarum ATCC 14917. We found that calcium ions differentially affect both growth and biofilm formation of these species. In general, calcium supplementation promotes the growth of both species, albeit with some variations in the extent to which different growth parameters were impacted. Calcium ions strongly induce biofilm formation of L. acidophilus ATCC 4356 but not L. plantarum ATCC 14917. Based on bioinformatic analyses and experimental chelator studies, we hypothesize that surface proteins specific to L. acidophilus ATCC 4356, like S-layer proteins, are responsible for Ca2+-induced biofilm formation. The ability of bacteria to form biofilms has been linked with their ability to colonize in the gut microbiota. This work shows how metal ions like Ca2+ may be important not just as nutrients for bacteria growth, but also for their ability to facilitate cell-cell interactions and possibly colonization in the gut microbiota.

Gut microbiomes contribute to animal health and fitness. The immense biochemical diversity of bacteria holds particular potential for neutralizing environmental toxins and thus helping hosts deal with new toxic challenges. To explore this potential, we used Caenorhabditis elegans harboring a defined microbiome, and the antibiotic neomycin as a model toxin, differentially affecting microbiome strains, and also toxic to worms. Worms exposed to neomycin showed delayed development and reduced survival but were protected when colonized with neomycin-resistant Stenotrophomonas. 16S rRNA sequencing, bacterial load quantification, genetic manipulation, and behavioral assays showed that protection was linked to enrichment of Stenotrophomonas carrying a neomycin-modifying enzyme. Enrichment was facilitated by altered bacterial competition in the gut, as well as by KGB-1/JNK-dependent behavioral changes. While microbiome remodeling conferred toxin resistance, it was associated with reduced infection resistance and metabolic changes. These findings suggest that microbiome adaptation can help animals cope with stressors but may have long-term consequences that add to effects of direct intoxication.

Fungi are important and often underestimated human pathogens. Infections with fungi mostly originate from the environment, from soil or airborne spores. By contrast, Candida albicans, one of the most common and clinically important fungal pathogens, permanently exists in the vast majority of healthy individuals as a member of the human mucosal microbiota. Only under certain circumstances will these commensals cause infections. However, although the pathogenic behaviour and disease manifestation of C. albicans have been at the centre of research for many years, its asymptomatic colonization of mucosal surfaces remains surprisingly understudied. In this Review, we discuss the interplay of the fungus, the host and the microbiome on the dualism of commensal and pathogenic life of C. albicans, and how commensal growth is controlled and permitted. We explore hypotheses that could explain how the mucosal environment shapes C. albicans adaptations to its commensal lifestyle, while still maintaining or even increasing its pathogenic potential.

The gut microbiome, a complex community of microorganisms residing in the intestinal tract, plays a dual role in colorectal cancer (CRC) development, acting both as a contributing risk factor and as a protective element. This review explores the mechanisms by which gut microbiota contribute to CRC, emphasizing inflammation, oxidative stress, immune evasion, and the production of genotoxins and microbial metabolites. Fusobacterium nucleatum, Escherichia coli (pks+), and Bacteroides fragilis promote tumorigenesis by inducing chronic inflammation, generating reactive oxygen species, and producing virulence factors that damage host DNA. These microorganisms can also evade the antitumor immune response by suppressing cytotoxic T cell activity and increasing regulatory T cell populations. Additionally, microbial-derived metabolites such as secondary bile acids and trimethylamine-N-oxide (TMAO) have been linked to carcinogenic processes. Conversely, protective microbiota, including Lactobacillus, Bifidobacterium, and Faecalibacterium prausnitzii, contribute to intestinal homeostasis by producing short-chain fatty acids (SCFAs) like butyrate, which exhibit anti-inflammatory and anti-carcinogenic properties. These beneficial microbes enhance gut barrier integrity, modulate immune responses, and inhibit tumor cell proliferation. Understanding the dynamic interplay between pathogenic and protective microbiota is essential for developing microbiome-based interventions, such as probiotics, prebiotics, and fecal microbiota transplantation, to prevent or treat CRC. Future research should focus on identifying microbial biomarkers for early CRC detection and exploring personalized microbiome-targeted therapies. A deeper understanding of host-microbiota interactions may lead to innovative strategies for CRC management and improved patient outcomes.

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.

Roux-en-Y gastric bypass (GBP) surgery is an effective treatment for reducing body weight and correcting metabolic dysfunction in individuals with severe obesity. Herein, we characterize the differences between very low energy diet (VLED) and GBP induced weight loss by multi-omic analyses of microbiome and host features in a non-randomized, controlled, single-center study. Eighty-eight participants with severe obesity were recruited into two arms - GBP versus VLED with matching weight loss for 6 weeks and 2-years of follow-up. A dramatic shift in the distribution of gut microbial taxa and their functional capacity was seen in the GBP group at Week 2 after surgery and was sustained through 2 years. Multi-omic analyses were performed after 6 weeks of matching weight loss between the GBP and VLED groups, which pointed to microbiome derived metabolites such as indoxyl sulphate as characterizing the GBP group. We also identified an inverse association between Streptococcus parasanguinis (an oral commensal) and plasma levels of tryptophan and tyrosine. These data have important implications, as they reveal a significant robust restructuring of the microbiome away from a baseline dysbiotic state in the GBP group. Furthermore, multi-omics modelling points to potentially novel mechanistic insights at the intersection of the microbiome and host.

To explore the correlation of dietary index for gut microbiota (DI-GM) with non-alcoholic fatty liver disease (NAFLD).

Data of 6,711 participants were extracted from the National Health and Nutrition Examination Survey (NHANES) during 2007-2018. A weighted logistic regression analysis was employed for assessment of the correlation of DI-GM with NAFLD, and a restricted cubic spline (RCS) analysis was implemented to examine potential non-linear associations. Subgroup analyses were conducted to identify particularly susceptible groups. Additionally, the synergistic effects of different DI-GM components on NAFLD risk was assessed by weighted quantile sum (WQS) regression.

The DI-GM exhibited statistically significant correlation with NAFLD [OR (95%CI):0.91 (0.85, 0.98), p = 0.015]. The results of the RCS analysis indicated a linear correlation of DI-GM and NAFLD (p = 0.810 for non-linearity). Further stratified analyses indicated that the negative correlation of DI-GM with NAFLD were significant and consistent for all subgroups. The results of WQS regression revealed that soybean (27%), refined grains (17%), coffee (16%), and red meat (9%) had the highest contribution weights to NAFLD.

As an important tool for assessment of the influences of diet on gut microbiota, DI-GM is negatively correlated with NAFLD risk factors. Soybean, refined grains, coffee, and red meat are key factors influencing NAFLD. The direct correlation of DI-GM with NAFLD shall be explored and the effectiveness of prevention and treatment of NAFLD shall be evaluated by improving DI-GM scores via dietary interventions.

Erucic acid (EA) is a monounsaturated fatty acid primarily consumed as rapeseed oil and mustard oil (MO). The consumption of EA-rich food has been reported to have adverse effects on health, particularly myocardial lipidosis and hepatic steatosis. Consequently, several countries, including the United States, European countries, New Zealand, and Australia, set limits on their daily intake. However, EA-rich MO (30%-50%) is still consumed in Asia. In contrast, limited studies on humans have reported a protective role of MO in acute myocardial infarction, ischemic heart disease, and neurologic disorders. The previous studies have shown the association of EA with both beneficial and adverse effects. Therefore, a comprehensive review of EA will help us understand its effect on health. Because EA consumption is banned in some countries, a detailed and updated review on EA might help us understand its role as a toxicant or therapeutic.

The intestinal microbiota is a key environmental factor in the development of colorectal cancer (CRC). Here, we report that, in the context of mild colonic inflammation, the microbiota protects against colorectal tumorigenesis in mice. This protection is achieved by microbial suppression of the long non-coding RNA (lncRNA) Snhg9. Snhg9 promotes tumor growth through inhibition of the tumor suppressor p53. Snhg9 suppresses p53 activity by dissociating the p53 deacetylase sirtuin 1 (SIRT1) from the cell cycle and apoptosis regulator 2 (CCAR2). Consequently, the depletion of the microbiota by antibiotics causes upregulation of Snhg9 and accelerates CRC progression. Moreover, Snhg9 is functionally conserved. Human SNHG9 promotes tumor growth via the same mechanism as mouse Snhg9, despite their low sequence similarity.

Few epidemiological evidence has focused on the impact of organophosphate esters (OPEs) and the risk of eczema, and underlying role of gut microbiota. Based on the Shanghai Maternal-Child Pairs Cohort, a nested case-control study including 332 eczema cases and 332 controls was conducted. Umbilical cord blood and stools were collected for OPEs detection and gut microbiota sequencing, separately. Eczema cases were identified using the International Study of Asthma and Allergies in Childhood core questionnaire and clinical diagnosis. The environmental risk score (ERS) for OPEs was developed to quantify OPEs burden. Conditional logistic regression models, multivariate analysis by linear models, negative-binomial hurdle regression, and mediation analysis were employed. Tris(2-butoxyethyl) phosphate (TBP), tris (2-butoxy ethyl) phosphate (TBEP), 2-ethylhexyl diphenyl phosphate (EHDPP), and tris(1,3-dichloro-2-propyl) phosphate (TDCPP) had detection rates > 50 %, with median concentrations ranged from 0.11 to 2.71 μg/L. TBP (OR = 1.12, 95 % CI: 1.01, 1.25), TDCPP (OR = 1.32, 95 % CI: 1.09, 1.59), and ERS (OR = 6.44, 95 % CI: 3.47, 11.94) were associated with elevated risk of eczema. OPEs exposure was correlated with increased alpha diversity and the abundance of several pathogenic bacteria, such as Klebsiella. Negative associations were observed between OPEs exposure and the abundances of Lachnospiraceae genera. Additionally, a positive correlation was identified between alpha diversity and the risk of eczema during childhood. Alpha diversity indices and Lachnospiraceae serve as significant mediators in this relationship. Results of this study indicate that prenatal exposure to OPEs is linked to an elevated risk of eczema and gut microbiota dysbiosis, potentially contributing to immunotoxicity of OPEs during early life.

Bivalve microbiota play a vital role in host health, supporting nutrient processing, immunity, and disease resistance. However, the increasing hypoxia in Chilean coastal waters, caused by climate change and eutrophication, threatens to disrupt this microbial balance, potentially promoting pathogens and impairing essential functions. Mytilus chilensis is vulnerable to hypoxia-reoxygenation cycles, yet the effects on its microbiota remain poorly understood. This study investigates the impact of hypoxia on the structure and functional potential of the microbial communities residing in the gills and digestive glands of M. chilensis. Employing full-length 16S rRNA gene sequencing, we explored hypoxia's effects on microbial diversity and functional capacity. Our results revealed significant alterations in the microbial composition, with a shift towards facultative anaerobes thriving in low oxygen environments. Notably, there was a decrease in dominant bacterial taxa such as Rhodobacterales, while opportunistic pathogens such as Vibrio and Aeromonas exhibited increased abundance. Functional analysis indicated a decline in critical microbial functions associated with nutrient metabolism and immune support, potentially jeopardizing the health and survival of the host. This study sheds light on the intricate interactions between host-associated microbiota and environmental stressors, underlining the importance of managing the microbiota in the face of climate change and aquaculture practices.

Hepatocellular carcinoma (HCC) is closely linked to alterations in the gut microbiota. This dysbiosis is characterized by significant changes in the microbial population, which correlate with the progression of HCC. Gut dysbiosis ultimately promotes HCC development in several ways: it damages the integrity of the gut-vascular barrier (GVB), alters the tumor microenvironment (TME), and even affects the intratumoral microbiota. Subsequently, intratumoral microbiota present a characteristic profile and play an essential role in HCC progression mainly by causing DNA damage, mediating tumor-related signaling pathways, altering the TME, promoting HCC metastasis, or through other mechanisms. Both gut microbiota and intratumoral microbiota have dual effects on HCC progression; a comprehensive understanding of their complex biological roles will provide a theoretical foundation for potential clinical applications in HCC treatment.

Alterations in the composition and function of the intestinal microbiota have been observed in organismal aging across a broad spectrum of animal phyla. Recent findings, which have been derived mostly in simple animal models, have even established a causal relationship between age-related microbial shifts and lifespan, suggesting microbiota-directed interventions as a potential tool to decelerate aging processes. To test whether a life-long microbiome rejuvenation strategy could delay or even prevent aging in non-ruminant mammals, we performed recurrent fecal microbial transfer (FMT) in mice throughout life. Transfer material was either derived from 8-week-old mice (young microbiome, yMB) or from animals of the same age as the recipients (isochronic microbiome, iMB) as control. Motor coordination and strength were analyzed by rotarod and grip strength tests, intestinal barrier function by serum LAL assay, transcriptional responses by single-cell RNA sequencing, and fecal microbial community properties by 16S rRNA gene profiling and metagenomics.

Colonization with yMB improved coordination and intestinal permeability compared to iMB. yMB encoded fewer pro-inflammatory factors and altered metabolic pathways favoring oxidative phosphorylation. Ecological interactions among bacteria in yMB were more antagonistic than in iMB implying more stable microbiome communities. Single-cell RNA sequencing analysis of intestinal mucosa revealed a salient shift of cellular phenotypes in the yMB group with markedly increased ATP synthesis and mitochondrial pathways as well as a decrease of age-dependent mesenchymal hallmark transcripts in enterocytes and TA cells, but reduced inflammatory signaling in macrophages.

Taken together, we demonstrate that life-long and repeated transfer of microbiota material from young mice improved age-related processes including coordinative ability (rotarod), intestinal permeability, and both metabolic and inflammatory profiles mainly of macrophages but also of other immune cells. Video Abstract.

Antigen-specific recognition of microbiota by T cells enforces tolerance at homeostasis. Conversely, dysbiosis leads to imbalanced T-cell responses, triggering inflammatory and autoimmune diseases. Despite their significance, the identities of immunogenic microbial antigens remain largely enigmatic. Here, we leveraged a sensitive, unbiased, genome-wide screening platform to identify peptides from Akkermansia muciniphila (AKK) and Bacteroides thetaiotaomicron (BT) recognized by CD4+ T cells. The platform is based on screening peptide libraries using an NFAT-fluorescence reporter cell line transduced with a retrovirus encoding an MHC-TCR (MCR) hybrid molecule. We discovered several novel epitopes from AKK and BT. T-cell hybridomas reactive to AKK and BT bacteria demonstrated polyreactivity to microbiota-derived peptides in co-cultures with MCR reporter cells. Steady-state T cells recognized these epitopes in an MHC-restricted fashion. Intriguingly, most of the identified epitopes are broadly conserved within the given phylum and originate from membrane and intracellular proteins. Ex vivo stimulation of CD4+ T cells from mice vaccinated with the identified peptides revealed mono-specific IFN-γ and IL-17 responses. Our work showcases the potential of the MCR system for identifying immunogenic microbial epitopes, providing a valuable resource. Our study facilitates decoding antigen specificity in immune system-bacterial interactions, with applications in understanding microbiome and pathogenic bacterial immunity.

Ischemic stroke (IS) is a cerebrovascular disease that predominantly affects middle-aged and elderly populations, exhibiting high mortality and disability rates. At present, the incidence of IS is increasing annually, with a notable trend towards younger affected individuals. Recent discoveries concerning the "gut-brain axis" have established a connection between the gut and the brain. Numerous studies have revealed that intestinal microbes play a crucial role in the onset, progression, and outcomes of IS. They are involved in the entire pathophysiological process of IS through mechanisms such as chronic inflammation, neural regulation, and metabolic processes. Although numerous studies have explored the relationship between IS and intestinal microbiota, comprehensive analyses of specific microbiota is relatively scarce. Therefore, this paper provides an overview of the typical changes in gut microbiota following IS and investigates the role of specific microorganisms in this context. Additionally, it presents a comprehensive analysis of post-stroke microbiological therapy and the relationship between IS and diet. The aim is to identify potential microbial targets for therapeutic intervention, as well as to highlight the benefits of microbiological therapies and the significance of dietary management. Overall, this paper seeks to provide key strategies for the treatment and management of IS, advocating for healthy diets and health programs for individuals. Meanwhile, it may offer a new perspective on the future interdisciplinary development of neurology, microbiology and nutrition.

The interplay between nutrition and infectious diseases has been a central theme in health sciences for the last decades due to its great impact on the pediatric population, especially in immunocompromised patients and critically ill children. As conventional treatment and the development of antimicrobials for most infections standard treatment is either limited or not possible, alternative treatment options should be explored. Recent research shows that early enteral nutrition and nutritional supplements (such as probiotics and symbiotics) could have a pivotal role in promoting a healthy microbiome and subsequently preventing and improving outcomes for certain pediatric infectious diseases. However, understanding the specific mechanism of action and tailoring nutritional interventions remains a significant challenge. The optimal dose range for different probiotic strains and prebiotics and the most effective combination for each treatment indication needs further investigation and is yet to be defined. Additionally, in the era of personalized medicine, goal- and patient-directed treatment are key to optimizing and improving outcomes and minimizing potential complications and side effects, especially in complex and immunocompromised patients. The main objectives of this narrative review are 1. to explore the relationship and the complex interactions between microbiota and the human immune system; 2. to describe the influence of nutrition on infectious diseases; 3. to evaluate the impact of supplementation with probiotics and symbiotics in the prevention and treatment of the most relevant infections in children; and 4. to identify knowledge gaps and potential research priorities regarding the use of these supplements in pediatric patients.

Alterations in goblet cell biology constitute one of the most effective host responses against enteric parasites. In the gastrointestinal (GI) tract, millions of bacteria influence these goblet cell responses by binding to pattern recognition receptors such as toll-like receptors (TLRs). Studies suggest that the gut microbiota also interacts bidirectionally with enteric parasites, including Trichuris muris. Here, we study the roles of T. muris-altered microbiota and the TLR2-SPDEF axis in parasitic host defense. In acute T. muris infection, we observed altered gut microbiota composition, which, when transferred to germ-free mice, resulted in increased goblet cell numbers, Th2 cytokines and Muc2 expression, as well as increased Tlr2. Further, antibiotic (ABX)-treated TLR2-/- mice, despite having received the same T. muris-altered microbiota, displayed diminished Th2 response, Muc2 expression, and, intriguingly, diminished SPDEF expression compared to wildtype counterparts. When infected with T. muris, SPDEF-/- mice exhibited a reduced Th2 response and altered microbial composition compared to SPDEF+/+, particularly on day 14 post-infection, and this microbiota was sufficient to alter host goblet cell response when transferred to ABX-treated mice. Taken together, our findings suggest the TLR2-SPDEF axis, via T. muris-induced microbial changes, is an important regulator of goblet cell function and host's parasitic defense.

Through the brain-gut-microbiome axis, myriad psychological functions that affect behavior share a dynamic, bidirectional relationship with the intestinal microbiome. Little is known about the relationship between personality-a stable construct that influences social- and health-related behaviors-and the bacterial ecosystem. The authors of this exploratory study examined the relationship between general and maladaptive personality traits and the composition of the gut microbiome.

In total, 105 psychiatric inpatients provided clinical data and fecal samples. Personality traits were measured with the five-factor model of personality, the Structured Clinical Interview for DSM-IV Axis II Personality Disorders, and the Personality Inventory for DSM-5; 16S ribosomal DNA sequencing and whole-genome shotgun sequencing methods were used on fecal samples. Machine learning (ML) was used to identify personality traits associated with bacterial variability and specific taxa.

Supervised ML techniques were used to classify traits of social detachment (maximum area under the receiver operating characteristic curve [AUROC]=0.944, R2>0.20), perceptual disturbance (maximum AUROC=0.763, R2=0.301), and hoarding behaviors (maximum AUROC=0.722) by using limited sets of discriminant bacterial species or genera. Established bacterial genera associated with psychosis (e.g., Peptococcus and Coprococcus) were associated with traits of perceptual disturbance. Hoarding behaviors were associated with a defined gut microbial composition that included Streptococcus, a known contributor to the development of pediatric autoimmune neuropsychiatric disorders.

Observations from this study are consistent with recent findings demonstrating person-to-person interactions as a mode of gut microbiome transmission. This study adds to the emerging literature on the intricate connections between brain and gut function, expanding the interdisciplinary field of psychiatric microbiology.

In addition to individual genetics, environmental factors (e.g., dietary changes) may influence host susceptibility to gastrointestinal infection through unknown mechanisms. Herein, we developed a model in which CBA/J mice, a genetically resistant strain that tolerates intestinal colonization by the enteric pathogen Salmonella Typhimurium (S. Tm), rapidly succumb to infection after exposure to a diet rich in L-amino acids (AA). In mice, S. Tm-gastroenteritis is restricted to the large intestine (cecum), limiting their use to understand S. Tm small intestine (ileum) colonization, a feature of human Salmonellosis. Surprisingly, CBA mice fed AA diet developed ileitis with enhanced S. Tm ileal colonization. Using germ-free mice and ileal-fecal slurry transplant, we found diet-mediated S. Tm ileal expansion to be microbiota-dependent. Mechanistically, S. Tm relied on Fructosyl-asparagine utilization to expand in the ileum during infection. We demonstrate how AA diet overrides host genetics by altering the gut microbiota's ability to prevent S. Tm ileal colonization.

The USA is home to 83-88 million dogs, with 3-7 million living in shelters. Shelter dogs move through the supply chain from their geographical origin to adoptive homes, with possible exposure to pathogens and shift in their gut microbiota. However, research in this area is limited. This study examined the effects of intestinal colonization by ESBL bacteria on gut taxa abundance, diversity, and functions in 52 shelter dogs of various ages, sexes, and fertility statuses.

We isolated fecal DNA, sequenced their 16S, processed the sequences using DADA2, identified taxa profiles in each dog by Phyloseq, and analyzed Chao1, Shannon, and Simpson alpha diversity by ggplot2 and Wilcoxon test. We analyzed beta diversity using Bray-Curtis dissimilarity matrix from the vegan package. Differential abundance of taxa, gut microbiome functions, and differential abundance of microbiome functions were analyzed using DESeq2, PICRUSt2, and ALDEx2, respectively, with Wilcoxon rank and Kruskal-Wallis tests for comparisons between dog groups.

Firmicutes (69.3%), Bacteroidota (13.5%), Actinobacteriota (6.77%), Proteobacteria (5.54%), and Fusobacteriota (4.75%) were the major phyla in the gut of shelter dogs. ESBL bacteria colonized dogs had reduced gut microbiota alpha diversity than non-colonized dogs. The abundance levels of the following phyla (Proteobacteria, Deferribacterota, Bacteroidota, Fusobacteriota, and Spirochaetota), class (Gammaproteobacteria, Bacteroidia, Deferribacteres, Brachyspirae, and Fusobacteria), and families (Enterobacteriaceae, Peptostreptococcaceae, Lactobacillaceae, Lachnospiraceae, Prevotellaceae, and Peptostreptococcaceae) were significantly (p < 0.05) varied between the two dog groups. Further stratified analysis by age, sex, and spaying/neutering status influenced the abundance of taxa in ESBL bacteria colonized dogs, indicating these covariates act as effect modifiers. Most gut metabolic and biosynthetic pathways were downregulated in ESBL bacteria colonized dogs compared to non-colonized dogs. However, alpha-linolenic acid metabolism and shigellosis, fluorobenzoate degradation, allantoin degradation, toluene degradation, glycol degradation, fatty acid and beta-oxidation, and glyoxylate metabolism bypass pathways were increased in dogs colonized by ESBL bacteria.

Colonization by ESBL bacteria marks altered gut microbiota. Dog's demography and fertility status modify the alterations, indicating host factors and ESBL bacteria interplay to shape gut microbiota. ESBL bacteria or other factors reprogram gut microbiome functions through down and upregulating multiple metabolic and biosynthesis pathways to promote ESBL bacteria colonization.

This study examined the effects of dietary crude protein (CP: 18%, 15%) and crude fat (EE: 8%, 4%) levels, and their interactions, on growth performance, nutrient digestibility, serum indices, and rectal fecal microbiota in sika deer fawns during early wintering. A two-month 2 × 2 factorial experiment was conducted using 32 healthy five-month-old male fawns randomly assigned to four groups: P18E8 (18% CP, 8% EE), P18E4 (18% CP, 4% EE), P15E8 (15% CP, 8% EE), and P15E4 (15% CP, 4% EE). The P18E4 group showed the highest total weight gain and average daily gain (p < 0.05), along with greater apparent digestibility of dry matter, crude protein, calcium, and fiber fractions (p < 0.05). Serum urea content was significantly lower in this group, indicating improved nitrogen utilization (p < 0.05). Dominant fecal microbiota at the phylum level across all groups included Firmicutes_A and Bacteroidota, with the P18E4 group showing a unique genus composition within Bacteroidota, known for enhancing fiber digestion. In summary, a diet with 18% CP and 4% EE optimized growth performance, nutrient digestibility, and gut microbiota composition, providing a strategy for improving the health and productivity of sika deer fawns during overwintering.

Colonization of co-evolved, species-specific microbes in early life plays a crucial role in gastrointestinal development and immune function. This study hypothesized that modern pig production practices have resulted in the loss of co-evolved species and critical symbiotic host-microbe interactions. To test this, we reintroduced microbes from wild boars (WB) into conventional piglets to explore their colonization dynamics and effects on gut microbial communities, metabolite profiles, and immune responses. At postnatal day (PND) 21, 48 piglets were assigned to four treatment groups: (i) WB-derived mixed microbial community (MMC), (ii) sow-derived MMC, (iii) a combination of WB and sow MMC (Mix), or (iv) Control (PBS). Post-transplantation analyses at PND 48 revealed distinct microbial communities in WB-inoculated piglets compared with Controls, with trends toward differentiation from Sow but not Mix groups. WB-derived microbes were more successful in colonizing piglets, particularly in the Mix group, where they competed with Sow-derived microbes. WB group cecal digesta enriched with Lactobacillus helveticus, Lactobacillus mucosae, and Lactobacillus pontis. Cecal metabolite analysis showed that WB piglets were enriched in histamine, acetyl-ornithine, ornithine, citrulline, and other metabolites, with higher histamine levels linked to Lactobacillus abundance. WB piglets exhibited lower cecal IL-1β and IL-6 levels compared with Control and Sow groups, whereas the Mix group showed reduced IFN-γ, IL-2, and IL-6 compared with the Sow group. No differences in weight gain, fecal scores, or plasma cytokines were observed, indicating no adverse effects. These findings support that missing WB microbes effectively colonize domestic piglets and may positively impact metabolite production and immune responses.IMPORTANCEThis study addresses the growing concern over losing co-evolved, species-specific microbes in modern agricultural practices, particularly in pig production. The implementation of strict biosecurity measures and widespread antibiotic use in conventional farming systems may disrupt crucial host-microbe interactions that are essential for gastrointestinal development and immune function. Our research demonstrates that by reintroducing wild boar-derived microbes into domestic piglets, these microbes can successfully colonize the gut, influence microbial community composition, and alter metabolite profiles and immune responses without causing adverse effects. These findings also suggest that these native microbes can fill an intestinal niche, positively impacting immune activation. This research lays the groundwork for future strategies to enhance livestock health and performance by restoring natural microbial populations that produce immune-modulating metabolites.

The development of novel ingestible sensors can aid physicians and patients in obtaining precise data on the health status of the gut at a local level. This in turn can facilitate earlier and more accurate disease diagnosis, improve the delivery of point-of-care medicine, and allow monitoring of the gastrointestinal (GI) tract status. This Tutorial overviews characteristics of the gut for inexpert readers and reviews emerging chemical sensing technologies for the GI tract from an analytical chemistry viewpoint.

The liver is the most commonly metastasized organ in colorectal cancer (CRC), and distant metastasis is the primary cause of mortality from CRC. In recent years, researchers have discovered that tumor cells create a "pre-metastatic niche (PMN)" favorable to metastasis before reaching the metastatic location. This review discusses the many processes and mechanisms that lead to PMN formation in CRC, including gut microbiota, stem cell stimulation, immunocyte interactions, and the induction of extracellular vesicles that carry important information. It examines research methods and diagnostic and therapeutic approaches for treating metastatic CRC with PMN. The crucial significance of PMN formation in metastatic CRC is also highlighted.

Breast cancer is the most commonly diagnosed cancer in women worldwide, with alcohol consumption recognized as a significant risk factor. While epidemiological studies consistently show a positive correlation between alcohol consumption and increased breast cancer risk, the underlying mechanisms remain unclear. Recent evidence suggests that the gut microbiome-the diverse collection of microorganisms, including bacteria, viruses, and fungi, residing in the gastrointestinal tract-plays a pivotal role in systemic health and disease. This is achieved through its regulation of key physiological processes such as metabolism, immune function, and inflammatory responses. Disruption of the gut microbiome (dysbiosis) has recently been implicated in the development of breast cancer. We hypothesized that alcohol exposure induces gut dysbiosis, which in turn drives systemic inflammation and carcinogenic processes. Previously, we demonstrated that alcohol exposure promotes mammary tumor growth and aggressiveness in MMTV-Wnt1 (Wnt1) transgenic mice, an established model for investigating mechanisms of alcohol-induced tumor promotion. In this study, we sought to determine whether alcohol exposure induces gut dysbiosis in adolescent and adult Wnt1 transgenic mice and their wild-type FVB counterparts. Our findings revealed that alcohol exposure significantly reduced microbiome richness in adult Wnt1 and FVB mice. Alcohol exposure also markedly altered microbiome composition in adolescents and adults in both strains. Additionally, we identified specific microbial taxa that were significantly affected by alcohol exposure. These results demonstrate that alcohol disrupts the gut microbiome in a preclinical breast cancer model, providing insights into the potential role of gut dysbiosis in alcohol-induced mammary tumor promotion and offering avenues for future research.

There is mounting evidence for the involvement of the immune system, neuroinflammation and disturbed gut microbiota, or dysbiosis, in attention-deficit/hyperactivity disorder (ADHD). Gut dysbiosis is strongly implicated in many physical, autoimmune, neurological, and neuropsychiatric conditions, however knowledge of its particular pathogenic role in ADHD is sparse. As such, this narrative review examines and synthesizes the available evidence related to inflammation, dysbiosis, and neural processes in ADHD. Minimal differences in microbiota diversity measures between cases and controls were found, however many relative abundance differences were observed at all classification levels (phylum to strain). Compositional differences of taxa important to key gut-brain axis pathways, in particular Bacteroides species and Faecalibacterium, may contribute to inflammation, brain functioning differences, and symptoms, in ADHD. We have identified one possible model of ADHD etiopathogenesis involving systemic inflammation, an impaired blood-brain barrier, and neural disturbances as downstream consequences of gut dysbiosis. Nevertheless, studies conducted to date have varied degrees of methodological rigour and involve diverse participant characteristics and analytical techniques, highlighting a need for additional research.