Induction of IL-8 by Chlamydia trachomatis through MAPK pathway rather than NF-kappaB pathway.
10.3969/j.issn.1672-7347.2010.04.005
- Author:
Fan CHEN
1
;
Wen CHENG
;
Saidan ZHANG
;
Guangming ZHONG
;
Ping YU
Author Information
1. Department of Cardiology, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Chlamydia Infections;
metabolism;
Chlamydia trachomatis;
physiology;
Epithelial Cells;
metabolism;
microbiology;
HeLa Cells;
Humans;
Interleukin-8;
biosynthesis;
NF-kappa B;
metabolism;
Signal Transduction;
p38 Mitogen-Activated Protein Kinases;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2010;35(4):307-313
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To determine the signaling pathway required for Chlamydial induction of IL-8 expression in epithelial cells.
METHODS:The production and localization of IL-8 in Chlamydia-infected Hela 229 cells were monitored using Western blot, immunoflourescence, and ELISA. Activation of MAPK and NF-kappaB signaling pathways were detected by Western blot and immunoflourescence. The effect of different signaling pathways on Chlamydia-induced Il-8 was measured by experiments of chemical inhibitors.
RESULTS:IL-8 was induced by Chlamydia and was time-dependant. Chlamydial infection activated MAPK/ERK and MAPK/p38 pathways but not NF-kappaB pathway. Chlamydial induction of IL-8 was blocked by small molecule inhibitors targeting the ERK and p38 pathways.
CONCLUSION:Chlamydia-induced IL-8 in cervical epithelial cells, the natural target cell type of Chlamydia trachomatis infection, is dependent on MAPK pathway but not NF-kappaB pathway, which provides important information for further understanding the molecular mechanism of Chlamydia-induced inflammatory pathologies.
