Intestinal Epithelial PTPN2 Limits Pathobiont Colonization by Immune-Directed Antimicrobial Responses.

ABSTRACT:

Background and aims

Loss of activity of the inflammatory bowel disease (IBD) susceptibility gene, protein tyrosine phosphatase non-receptor type 2 (PTPN2), is associated with altered microbiome composition in both human subjects and mice. Further, expansion of the bacterial pathobiont, adherent-invasive E. coli (AIEC), is strongly linked to IBD pathogenesis. The mechanism by which intestinal epithelial cells (IEC) maintain equilibrium between commensal microbiota and immune cells to restrict invading pathobionts is poorly understood. Here, we investigated the role of IEC-specific PTPN2 in regulating AIEC colonization.

Methods

Tamoxifen-inducible, intestinal epithelial cell-specific Ptpn2 knockout mice (Ptpn2 ^ΔIEC) and control Ptpn2</

SUBMITTER: Chatterjee P 

PROVIDER: S-EPMC11463449 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature