Epithelial p38α Controls Immune Cell Recruitment in the Colonic Mucosa

PLoS Pathogens

Young Jun Kang¹  Jiahuai Han¹  Motoyuki Otsuka¹  Arjen van den Berg¹  Peter S. Tobias¹  Bruce A. Vallance²  Zhe Huang³  Duan-Wu Zhang³  Xiurong Wu³  Lixin Hong³ 

[1] Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, United States of America;Division of Gastroenterology, BC Children's Hospital, Vancouver, British Columbia, Canada;The Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University, Xiamen, Fujian, China

关键词: Colon;    Epithelial cells;    Gastrointestinal tract;    Immune cells;    Mouse models;    T cells;    Inflammation;    Cell staining;   

DOI  :  10.1371/journal.ppat.1000934

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

Intestinal epithelial cells (IECs) compose the first barrier against microorganisms in the gastrointestinal tract. Although the NF-κB pathway in IECs was recently shown to be essential for epithelial integrity and intestinal immune homeostasis, the roles of other inflammatory signaling pathways in immune responses in IECs are still largely unknown. Here we show that p38α in IECs is critical for chemokine expression, subsequent immune cell recruitment into the intestinal mucosa, and clearance of the infected pathogen. Mice with p38α deletion in IECs suffer from a sustained bacterial burden after inoculation with Citrobacter rodentium. These animals are normal in epithelial integrity and immune cell function, but fail to recruit CD4+ T cells into colonic mucosal lesions. The expression of chemokines in IECs is impaired, which appears to be responsible for the impaired T cell recruitment. Thus, p38α in IECs contributes to the host immune responses against enteric bacteria by the recruitment of immune cells.

【 授权许可】

CC BY