<i>Clostridioides difficile</i> toxins alter host metabolic pathway and bile acid homeostasis gene expression in colonic epithelium.

ABSTRACT: A major risk factor for acquiring Clostridioides difficile is antibiotic usage that disrupts a healthy microbial gut community, facilitating the establishment of infection. Once established, C. difficile secretes exotoxins (TcdA and TcdB) that are internalized into host colonic epithelial cells where they disrupt gut barrier function and induce hyperinflammation resulting in severe diarrhea and possibly leading to death. We employed three different platforms to explore gene expression of cells in the gut when exposed to C. difficile or its toxins, TcdA and TcdB. An antibiotic-treated mouse model of Clostridioides difficile infection (CDI) was used to identify differential gene expression with a NanoString Technologies mouse inflammatory gene panel consisting of

SUBMITTER: Thomas SA 

PROVIDER: S-EPMC12341375 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature