CCR2 mediates Helicobacter pylori-induced immune tolerance and contributes to mucosal homeostasis.

ABSTRACT:

Background

We previously demonstrated that H. pylori infection leads to increased induction of regulatory T cells in local and systemic immune compartments. Here, we investigate the role of CCR2 in the tolerogenic programing of dendritic cells in a mouse model of H. pylori infection.

Materials and methods

CCR2 deficient (CCR2KO) mice and wild-type (Wt) mice infected with H. pylori SS1 strain were analyzed by qPCR and FACS analysis. In vitro, bone marrow-derived DC on day 6 from CCR2KO and Wt mice cocultured with or without H. pylori were examined to determine the impact of CCR2 signaling on dendritic cells function by qPCR, ELISA, and FACS analyses.

Results

Acute H. pylori infection was associated with a threefold increase in CCR2 mRNA expression in the gastric mucosa

SUBMITTER: Sun X 

PROVIDER: S-EPMC5352485 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature