Ontology highlight
ABSTRACT: Methods
Colitis was induced in mice using 2,4,6-trinitrobenzene-sulfonic acid (TNBS), and mice were subsequently treated with either a PD-1 inhibitor or 5-amino-salicylic acid (ASA) as a positive control. Body weight, disease activity index (DAI), colon length, and tissue damage were evaluated, and the enteric microbiota was profiled using high-throughput 16S rRNA sequencing of fecal samples from the experimental mice.Results
TNBS caused mice to experience IBD-like symptoms, which were attenuated by the PD-1 inhibitor, as indicated by a decrease in DAI scores (p = 0.0002). Furthermore, in this mouse model of IBD, PD-1 inhibition improved the alpha diversity as well as restored the beta diversity of the enteric microbiome. It also significantly enriched the abundance of short-chain fatty acid- (SCFA-) producing bacteria of the Firmicutes (p < 0.05) and Bacteroidetes (p < 0.05) phyla but depopulated Proteobacteria (p < 0.05).Conclusion
PD-1 inhibition can partly mitigate TNBS-induced colitis and restore the enteric microbiota by enriching the abundance of SCFA-producing bacteria.
SUBMITTER: Xu HM
PROVIDER: S-EPMC7810563 | biostudies-literature | 2021
REPOSITORIES: biostudies-literature
Xu Hao-Ming HM Zhou You-Lian YL Xu Jing J Li Ying-Fei YF Zhao Chong C Huang Hong-Li HL Du Yan-Lei YL He Jie J Zhou Yong-Jian YJ Nie Yu-Qiang YQ
BioMed research international 20210107
<h4>Methods</h4>Colitis was induced in mice using 2,4,6-trinitrobenzene-sulfonic acid (TNBS), and mice were subsequently treated with either a PD-1 inhibitor or 5-amino-salicylic acid (ASA) as a positive control. Body weight, disease activity index (DAI), colon length, and tissue damage were evaluated, and the enteric microbiota was profiled using high-throughput 16S rRNA sequencing of fecal samples from the experimental mice.<h4>Results</h4>TNBS caused mice to experience IBD-like symptoms, whic ...[more]