Escherichia coli HPI-induced duodenitis through ubiquitin regulation of the TLR4/NF-κB pathway.

ABSTRACT:

Background

The Highly Pathogenic Island (HPI) found in Yersinia pestis can be horizontally transferred to E. coli, enhancing its virulence and pathogenicity. Ubiquitin (Ub) acts as an activator of the NF-κB pathway and plays a critical role in the inflammatory response. However, the precise mechanism by which Ub and the regulated TLR4/NF-κB pathway contribute to HPI-induced intestinal inflammation in E. coli remains unclear.

Results

In this study, we established Ub overexpression models of small intestinal epithelial cells (in vitro) and BALB/c mice (in vivo) and infected these models with HPI-rich E. coli. We investigated the role of the Ub-regulated TLR4/NF-κB pathway in E. coli HPI-induced intestinal inflammation through qPCR, ELISA, immunofluorescence, immunohistochemist

SUBMITTER: Zhao J 

PROVIDER: S-EPMC11829554 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature