
The Deletion of IL-17A Enhances Helicobacter hepaticus Colonization and Triggers Colitis
Author(s) -
Liqi Zhu,
Zhihao Wu,
Chen Zhu,
Jun Yin,
YouGui Huang,
Jie Feng,
Quan Zhang
Publication year - 2022
Publication title -
journal of inflammation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.656
H-Index - 33
ISSN - 1178-7031
DOI - 10.2147/jir.s359100
Subject(s) - colitis , mucus , inflammatory bowel disease , biology , pathogenesis , immunology , helicobacter , crypt , microbiology and biotechnology , helicobacter pylori , pathology , medicine , disease , endocrinology , ecology , genetics
IL-17 is a key regulator of the inflammatory response, and as such, it is involved in the constraint and clearance of pathogens. The mechanism of IL-17 in the pathogenesis of inflammatory bowel disease (IBD) caused by microbial infection is still unclear. Helicobacter hepaticus infection can induce colitis in many mouse strains, and thus, it has been widely used in the study of IBD pathogenesis.