Inflammatory bowel disease (IBD) is a recurring inflammatory disease of the gastrointestinal tract with unclear etiology, but it is thought to be related to factors like immune abnormalities and gut microbial dysbiosis. Probiotics can regulate host immunity and gut microbiota; thus, we investigated the alleviation effect and mechanism of the strain Lactobacillus gasseri G098 (G098) on dextran sodium sulfate (DSS)-induced colitis in mice. Three groups of mice (n = 8 per group) were included: normal control (NC), DSS-induced colitis mice (DSS), and colitis mice given strain (G098). Our results showed that administering G098 effectively reversed DSS-induced colitis-associated symptoms (mitigating weight loss, reducing disease activity index and pathology scores; p < 0.05 in all cases) and prevented DSS-induced mortality (62.5% in DSS group; 100% in G098 group). The mortality rate and symptom improvement by G098 administration was accompanied by a healthier serum cytokine balance (significant decreases in serum pro-inflammatory factors, interleukin (IL)-6 [p < 0.05], IL-1β [p < 0.01], and tumor necrosis factor (TNF)-α [p < 0.001], and significant increase in the serum anti-inflammatory factor IL-13 [p < 0.01], compared with DSS group) and gut microbiome modulation (characterized by a higher gut microbiota diversity [p < 0.05], significantly more Firmicutes and Lachnoclostridium [p < 0.05], significantly fewer Bacteroidetes [p < 0.05], and significant higher gene abundances of sugar degradation-related pathways [p < 0.05], compared with DSS-treated group). Taken altogether, our results suggested that G098 intake could mitigate DSS-induced colitis through modulating host immunity and gut microbiome, and strain treatment is a promising strategy for managing IBD.

The gut microbiota plays a significant role in tumor pathogenesis by regulating the host metabolism and immune response, and there are few studies focused on tracking changes in the gut microbiota from the onset of lung cancer. Therefore, the aim of our study is combining preclinical and clinical research to thoroughly analyze the signatures of fecal microbiota in lung cancer, which will be useful for early diagnosis and predicting the therapeutic efficacy of lung cancer. The first part of this study analyzed the fecal metagenomic differences between patients with non-small cell lung cancer and healthy subjects, and the second part of this work constructed a murine lung cancer model to monitor changes in mouse fecal metagenomics and T cell immunology during lung cancer progression. We found that the fecal microbiota was altered in both humans and mice with lung cancer, characterized by a significantly reduced microbial diversity and number of beneficial microbes, with increases in potential pathogens. The fecal level of Akkermansia muciniphila and the gut metabolic module of the secondary bile acid metabolism were diminished in both humans and mice with lung cancer compared with healthy subjects. Splenomegaly was observed in the lung cancer mice. Flow cytometer analysis of the splenocytes revealed substantial alterations in the proportions of T cell subsets in the lung cancer mice, characterized by significant increases in CD4⁺Foxp3⁺CD25⁺ T regulatory cells (p < 0.05) while significant decreases in CD3⁺ T cells (p < 0.001), CD4⁺ T cells (p < 0.001), and the CD4⁺/CD8⁺ ratio (p < 0.01). Vertical and longitudinal analyses of the fecal microbiota of the two mouse groups identified some lung cancer biomarkers (including Acutalibacter timonensis, Lachnospiraceae bacterium NSJ-38 sp014337195, etc.). The fecal microbiota of the lung cancer mice had a reduced metagenomic potential for neurotransmitters (melatonin, γ-aminobutyric acid, and histamine) compared with healthy mice. In summary, this study found that the diversity, structure, and composition of gut microbiota vary between cancer and healthy conditions, ultimately leading to changes in the potential for functional metagenomics.

Inflammatory bowel disease (IBD) is a chronic non-specific gut inflammatory disease. Conventional treatments are insufficient to support long-term disease remission, so there is an urgent need to search for new IBD treatment options. This study evaluated the alleviation effect of Lactobacillus (L.) helveticus H9 on dextran sodium sulfate (DSS)-induced colitis rats. We found that administering L. helveticus H9 significantly reduced DAI (disease activity index) scores (p ≤ 0.05), spleen weights (p ≤ 0.05), and colonic tissue damage in the colitis rats, while increasing the body weight gain rate. Compared with the DSS group, L. helveticus H9-receiving rats had less serum tumor necrosis factor-α (p ≤ 0.05) and interleukin-1β (p < 0.01), a higher gut microbiota diversity, and significantly more Alistipes senegalensis (p ≤ 0.05) and Parabacteroides distasonis (p < 0.01). On the metabolomics level, 65 significantly differential metabolites (VIP > 1, p < 0.05, fold change > 2 or <0.5) were identified between the probiotic and DSS groups. Some significantly enriched pathways were identified in the fecal metabolome of the probiotic group, including Sphingolipid metabolism, Linoleic acid metabolism, alpha-Linolenic acid metabolism, Arachidonic acid metabolism, Glycerophospholipid metabolism, Pyrimidine metabolism, Tryptophan metabolism, Fatty acid biosynthesis and Steroid hormone biosynthesis metabolic pathways, and lecithin is an important differential metabolite interconnecting several of the enriched pathways. In summary, administering L. helveticus H9 modulated the gut microbiota, metabolome, and host immune response, which could relate to symptom alleviation in the colitis rats. Our study provides interesting data regarding the use of probiotics in managing chronic colitis.