Loss of NOD2 in macrophages improves colitis and tumorigenesis in a lysozyme-dependent manner.

ABSTRACT:

Background

Crohn's disease (CD) is a complex and poorly understood myeloid-mediated disorder. Genetic variants with loss of function in the NOD2 gene confer an increased susceptibility to ileal CD. While Nod2 in myeloid cells may confer protection against T-cell mediated ileopathy, it remains unclear whether it may promote resolution of the inflamed colon. In this study, we evaluated the function of Nod2 in myeloid cells in a model of acute colitis and colitis-associated colon cancer (CAC).

Methods

To ablate Nod2 specifically within the myeloid compartment, we generated LysM^Cre/+;Nod2^fl/fl mice. The role of NOD2 was studied in a setting of Dextran Sodium Sulfate (DSS)-induced colitis and in azoxymethane (AOM)/DSS model. Clinical parameters

SUBMITTER: Chauvin C 

PROVIDER: S-EPMC10590911 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature