Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with gut dysbiosis. This study aimed to investigate the effects of heat-killed Bifidobacterium bifidum B1628 (HB1628) in dextran sulfate sodium (DSS)-induced colitis in mice. The following three mouse groups were included (n = eight per group): NC (normal control), DSS (colitis), and HB1628 (colitis and postbiotic). The mice in the DSS group showed significant weight loss and histological damage, developed bloody diarrhea, scored high in the disease activity index (DAI), and exhibited increases in pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF]-α) and decreases in an anti-inflammatory cytokine (IL-13) in the serum. These changes were accompanied by gut microbiota modulation in colitis mice (decreases in Rikenellaceae and Eubacterium; increases in Peptostreptococcaceae, Bacteroides vulgatus, and Parasutterella excrementihominis). The HB1628 group had lower DAIs, histology scores, and serum levels of pro-inflammatory cytokines (IL-1β and TNF-α), but higher levels of an anti-inflammatory cytokine (IL-13), compared with the DSS group, suggesting a less severe inflammatory state after the HB1628 intervention. Additionally, HB1628 improved DSS-induced gut dysbiosis, which is evidenced by increases in intestinal beneficial bacteria, such as Lactobacillus, and decreases in known unfavorable taxa in IBD, e.g., Porphyromonadaceae, Subdoligranulum, Lachnospiraceae bacterium 3_1_46FAA, and Alistipes indistinctus. Functional metagenomics revealed three significantly enriched metabolic pathways in the HB1628 group (namely, the aerobic respiration I [cytochrome c] pathway and the superpathways of L-phenylalanine biosynthesis and L-tryptophan biosynthesis, respectively). In conclusion, our results showed that HB1628 effectively improved the inflammation state and tissue damage in DSS-induced colitis mice, and the symptom relief effect was accompanied by obvious gut microbiota remodulation.

Gut microbial dysbiosis, especially bacteriome, has been implicated in Alzheimer’s disease (AD). However, nonbacterial members of the gut microbiome in AD, such as the mycobiome, archaeome, and virome, are unexplored. Here, we perform higher-resolution shotgun metagenomic sequencing on fecal samples collected longitudinally from a mouse model of AD to investigate longitudinal and multi-kingdom gut microbiome profiling. Shotgun metagenomic sequencing of fecal samples from AD mice and healthy mice returns 41,222 bacterial, 414 fungal, 1836 archaeal, and 1916 viral species across all time points. The ecological network pattern of the gut microbiome in AD mice is characterized by more complex bacterial–bacterial interactions and fungal–fungal interactions, as well as simpler archaeal–archaeal interactions and viral–viral interactions. The development of AD is accompanied by multi-kingdom shifts in the gut microbiome composition, as evidenced by the identification of 1177 differential bacterial, 84 differential fungal, 59 differential archaeal, and 10 differential viral species between healthy and AD mice across all time points. In addition, the functional potential of the gut microbiome is partially altered in the development of AD. Collectively, our findings uncover longitudinal and multi-kingdom gut microbiome alterations in AD and provide a motivation for considering microbiome-based therapeutics during the prevention and treatment of AD.

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.