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J Immunol. 2013 Sep 1;191(5):2764-2770. doi: 10.4049/jimmunol.1300908. Epub 2013 Aug 5.

Activation of p38α in T cells regulates the intestinal host defense against attaching and effacing bacterial infections.

Author information

Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037.
Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Division of Gastroenterology, BC Children's Hospital, Vancouver, British Columbia, Canada State Key.
State Key Laboratory of Cellular Stress Biology and School of Life Sciences, Xiamen University, Xiamen, Fujian, China.
Contributed equally


Intestinal infections by attaching and effacing (A/E) bacterial pathogens cause severe colitis and bloody diarrhea. Although p38α in intestinal epithelial cells (IEC) plays an important role in promoting protection against A/E bacteria by regulating T cell recruitment, its impact on immune responses remains unclear. In this study, we show that activation of p38α in T cells is critical for the clearance of the A/E pathogen Citrobacter rodentium. Mice deficient of p38α in T cells, but not in macrophages or dendritic cells, were impaired in clearing C. rodentium. Expression of inflammatory cytokines such as IFN-γ by p38α-deficient T cells was reduced, which further reduced the expression of inflammatory cytokines, chemokines, and antimicrobial peptide by IECs and led to reduced infiltration of T cells into the infected colon. Administration of IFN-γ activated the mucosal immunity to C. rodentium infection by increasing the expression of inflammation genes and the recruitment of T cells to the site of infection. Thus, p38α contributes to host defense against A/E pathogen infection by regulating the expression of inflammatory cytokines that activate host defense pathways in IECs.

[Indexed for MEDLINE]
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