Akkermansia, a next-generation probiotic candidate, exhibits a reduced abundance in obesity yet persists in the gut, suggesting unique adaptive mechanisms for survival in this adverse metabolic environment. To elucidate these mechanisms, a comparative pan-genome analysis of 494 Akkermansia metagenome-assembled genomes from hosts with diverse body mass indices was conducted. It was found that the genus possesses high genetic diversity, with Akkermansia muciniphila as the dominant species (80%), though species distribution itself was not correlated with BMI. There were 15 genes significantly enriched in obese individuals. These genes may potentially be involved in pathways such as nutrient acquisition, antioxidant stress response, energy metabolism, translational fidelity, and viral defense. Co-occurrence network analysis showed that these genes are associated with pathways including the tricarboxylic acid cycle and lipoic acid metabolism. These findings suggest potential adaptive functional mechanisms of Akkermansia for survival in the obese gut environment, providing novel insights for the development of targeted probiotics addressing obesity-related conditions.

Bifidobacterium bifidum is recognized for its immunomodulatory potential, yet the specific components mediating its anti-inflammatory effects remain poorly defined. Here, we systematically dissected the role of B. bifidum-derived lipoteichoic acid (LTA) in modulating mucosal immunity and alleviating 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced acute colitis. Initial in vitro assays revealed that the IL-10-inducing activity of B. bifidum in mesenteric lymph node cells resides mainly in heat-resistant cell wall fractions, particularly LTA, acting through a TLR2-associated (and pharmacologically TLR2-sensitive) pathway. Comparative analyses among multiple B. bifidum strains demonstrated that LTA immunostimulatory potency strongly predicted protective efficacy against colitis, with FJSWX19M5 strain LTA exerting the most pronounced anti-inflammatory effects in both conventional and germ-free mouse models. In vivo, mice received LTA by oral gavage (0.2 mg/mouse, 200 μL) prior to TNBS challenge. LTA from FJSWX19M5 significantly improved survival, ameliorated colonic injury and inflammation, reduced IL-1β production, and modulated Treg cell distribution, outperforming other strain LTAs. Transcriptomic profiling showed that FJSWX19M5 LTA intervention prominently altered colonic gene expression, activating multiple immune- and inflammation-related signaling pathways, such as Jak-STAT, PI3K-Akt, and IL-17. Furthermore, FJSWX19M5 LTA enhanced both T and B lymphocyte proliferation and cellular immunity in healthy mice. Together, these results establish that the anti-colitis and immunoregulatory benefits of B. bifidum are largely attributable to strain-specific LTA, highlighting its mechanistic link to TLR2-involved mucosal immune modulation and supporting its potential as a defined immunomodulatory molecule for IBD-relevant intervention.

Lactobacilli with different lifestyles show different ecological adaptabilities and host interaction abilities in the intestine. This study conducted a comparative genome analysis of 232 strains of lactobacilli, combined with carbohydrate-active enzyme and colonization factor analysis, and found that the genome of free-living lactobacilli is larger than that of host-adapted lactobacilli and the CAZymes spectrum is closely related to its lifestyle. In vivo experiments showed that host-adapted lactobacilli have significantly better colonization ability in the intestine than nomadic lactobacilli, and can still maintain a high number of live bacteria after stopping intake. Single-cell transcriptome technology was further used to explore the effects of lactobacilli intake on intestinal cells from the host perspective, and it was found that epithelial cells and immune cells (especially T cells and B cells) were most significantly affected by lactobacilli. Specifically, host-adapted lactobacilli (such as Lactobacillus reuteri) showed stronger anti-inflammatory effects in regulating Cd4+Tn cells, Cd4+Th/Treg cells, and Cd8ααT cells, and significantly downregulated the differentiation of pro-inflammatory cells such as Th1, Th2, and Th17. These findings not only clarify the relationship between Lactobacillus lifestyle and its genomic characteristics, colonization ability and immunomodulatory function, but also provide an important theoretical basis for the formulation of precise probiotic intervention strategies based on Lactobacillus.

Chemical hazards in foods have become a global public health challenge with the widespread use of chemicals in food processing. Currently, the effects of chemical exposure on human health are usually assessed by relying on complex and invasive assays for physiological and tissue parameters. As “the inhabitant” in the digestive tract, the gut microbiota has been the subject of numerous studies in recent years that suggest a possible link to food hazards. Changes in the abundance and function of the gut microbiota in response to foodborne contaminants may have the ability to determine the potential risk of food hazards. Non-invasive assays for the gut microbiota, a “microbial organ” sensitive to food safety hazards, have great potential for application in the safety risk assessment of chemical hazards in foods. In addition, the gut microbiota metabolizes and transforms certain chemicals and can also influence the toxicity and bioavailability of chemicals by modulating the host’s immune system, barrier function and metabolic pathways. Therefore, understanding the interaction between the gut microbiota and food hazards is important for assessing food safety and developing effective intervention strategies. This article reviews the applications, advantages, limitations and challenges of gut microbiota research models and omics technologies in the safety risk assessment of chemical hazards in foods. It aims to provide a scientific basis for the monitoring and risk assessment of food hazards and to provide new insights into the application of gut microbiota research models and omics techniques.

Antibiotic exposure has adverse effects on intestinal immunity, metabolism, and gut microbiota (GM) composition, particularly by disturbing GM composition without short-term recovery. Capsaicin, a dietary irritant, is generally avoided during antibiotic therapy, but its mechanism remains unclear. To explore the effects of capsaicin on intestinal health during antibiotic administration, we conducted experiments in specific pathogen free (SPF) and germ-free (GF) mice and correlation analyses using 16S rRNA sequencing and non-targeted metabolomics to explore the protective role of the intestinal biological barrier. The results showed that additional supplementation of capsaicin under antibiotic exposure did not cause serious damage to the intestine, but had potential adverse effects on the structure, function, and metabolites of GM, including increasing the abundance of opportunistic pathogens (Mucispirillum and Aeromonas), enriching metabolic pathways (arachidonic acid metabolism and lipopolysaccharide biosynthesis), and metabolites associated with colon inflammation (N-acetylhistamine). In the absence of GM barrier, the beneficial function of capsaicin on the intestine was weakened and even induced adverse effects, suggesting that GM may have a certain mediating mechanism in the physiological function of capsaicin.

Infancy and toddlerhood are critical phases of life, as the gut microbiota is established here, which influences current and future health. During this period, the microbiota was relatively less stable and highly responsive to environmental factors. Therefore, it is important to understand how dietary factors affect this complex stage of microbial assembly. The effect of feeding practices (breast milk/formula) on microbial colonization in early infancy has been actively studied; however, studies on the effect of diet on the gut microbiota during the complementary feeding period are sparse. The introduction of complementary foods provides abundant new dietary compounds for the gut microbiota, which induces a shift in gut microbiota and metabolism from milk-adapted toward a more mature and diverse adult-like community. Herein, we discuss the impact of dietary nutrients (carbohydrates, proteins, fats, vitamins, and minerals) on microbiome of infants and toddlers. Furthermore, this review summarizes the effects of complementary feeding patterns, specific foods (such as cereals; legumes and nuts; vegetables and fruits; meats; dairy products), food additives, and malnutrition (undernutrition or overnutrition) on gut microbiota of this populations. These findings might deepen our comprehension of the complex interactions between diets and the development and establishment of the gut microbiota. This may facilitate the tailoring of interventions aimed at promoting beneficial modifications within the gut microbial community. Furthermore, the insights gained could inform the design and implementation of safe and efficacious complementary feeding practices.