Protective Effects of a Novel Probiotic Bifidobacterium pseudolongum on the Intestinal Barrier of Colitis Mice via Modulating the Pparγ/STAT3 Pathway and Intestinal Microbiota

Abstract

Colitis has become a major health concern worldwide. The objective of the present study was to determine the probiotic influence of different strains of B. pseudolongum (Bp7 and Bp8) on alleviating colitis and to explore its possible potential mechanisms. Our results displayed that Bp7 and Bp8 intervention effectively reduced dextran sodium sulfate (DSS)-caused body weight loss and the release of several pro-inflammatory factors (interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α)) and increased the activities of antioxidant enzymes (T-AOC, SOD, and GSH) and the concentrations of tight junction proteins (occludin, claudin-1, and ZO-1). Moreover, Bp7 and Bp8 intervention drastically down-regulated the expression of colonic MyD88, NF-κB, iNOS and COX2 and drastically elevated the expression of colonic STAT3, Nrf2, and PPARγ. Gas chromatography-mass spectrometry results revealed that the cecal levels of isobutyric, butyric, and isovaleric acids were drastically increased in colitis mice intervened with Bp7 and Bp8. Moreover, 16S rRNA sequencing revealed that Bp7 and Bp8 intervention modulated the intestinal microbiota structure, particularly by enhancing the proportion of Eubacterium coprostanoligenes group, Marvinbryantia, Enterorhabdus, Faecalibaculum, Coriobacteriaceae UCG 002, Alistipes, and Bifidobacterium, which are relevant to the levels of cecal isobutyric acid, butyric acid, isovaleric acid, and inflammatory cytokines. Collectively, these findings suggest that Bp7 and Bp8 intervention alleviates the intestinal barrier function, possibly by blocking the secretion of proinflammatory cytokines, maintaining the intestinal physical barrier integrity, activating the PPARγ/STAT3 pathway, and modulating intestinal microbiota composition. Our study also suggested that B. pseudolongum is a promising probiotic for colitis treatment.

Bifidobacterium longum CCFM1206 Promotes the Biotransformation of Glucoraphanin to Sulforaphane That Contributes to Amelioration of Dextran-Sulfate-Sodium-Induced Colitis in Mice

“…The mRNA transcription levels of claudin-1, occludin, ZO-1, Iκ-Bα, NF-κB, Nrf-2, and NQO1 were estimated using a RT-qPCR system (Bio-Rad, Hercules, CA, U.S.A.). The gene sequences of the primers were obtained from the references and listed in Table . , …”

“…The gene sequences of the primers were obtained from the references and listed in Table 1. 16,17 Immunohistochemical Analysis. Immunohistochemical analysis was implemented as described by the research of Guo et al 18 Briefly, colon sections were incubated with primary antibodies against occludin, claudin-1, ZO-1, Nrf-2, phospho-Nrf2 (p-Nrf2), Iκ-Bα, NF-κB, and NQO1 for 60 min, followed by incubation with a secondary antibody and streptavidin−biotin peroxidase for 120 min.…”

Preventive effect of tilapia skin collagen hydrolysates on ulcerative colitis mice based on metabonomic and16 S rRNAgene sequencing

“…Furthermore, norank_f__Muribaculaceae was reported to produce SCFAs and was positively related to isovaleric acid; thus, there might be a positive correlation between the abundance of norank_f__Muribaculaceae and the content of isovaleric acid 45 . Allobaculum and unclassified_Ruminococcaceae are SCFAs‐producing bacteria, Enterorhabdus can hydrolyze primary bile acids and promote the egestion of bile acid; the high concentrations of secondary bile acid and SCFAs could increase the expression of P‐glycoprotein, which could defer the spread of inflammation and maintain the homeostasis of the intestinal environment 72,80 . Therefore, changes in the abundances of Escherichia‐Shigella , Allobaculum , unclassified_Ruminococcaceae , and Enterorhabdus may have an intimate relationship with the development of UC.…”

Lactobacillus paracasei CCFM1223 Protects against Lipopolysaccharide-Induced Acute Liver Injury in Mice by Regulating the “Gut–Liver” Axis

“…Immunohistochemical analysis was carried out as described in the previous report [ 14 ]. Briefly, partial liver tissues were harvested and incubated with a primary antibody to p65, Iκ-Bα, and Nrf2 for 60 min and then incubated with a secondary antibody and streptavidin-biotin peroxidase for 120 min.…”