Expression of Cyclooxygenase-2 in Human Intestinal Epithelial Cells Stimulated with Bacteroides fragilis Enterotoxin.
- Author:
Jung Mogg KIM
1
;
Shin Jae KANG
;
Soo Jin CHO
;
Hwoon Yong JUNG
;
Yu Kyoung OH
;
Young Jeon KIM
Author Information
1. Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Korea. jungmogg@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
Bacteroides fragilis enterotoxin;
Cyclooxygenase-2;
NF-kappaB;
Prostaglandin
- MeSH:
Bacteroides fragilis*;
Bacteroides*;
Blotting, Western;
Colon;
Cyclooxygenase 2*;
Dinoprostone;
Enterotoxins*;
Epithelial Cells*;
Humans*;
Inflammation;
Intestinal Mucosa;
L-Lactate Dehydrogenase;
NF-kappa B;
Prostaglandin-Endoperoxide Synthases;
Radioimmunoassay;
RNA, Messenger
- From:Journal of Bacteriology and Virology
2002;32(2):147-157
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
A ~20 kDa heat-labile toxin (BFT) produced by enterotoxigenic B. fragilis induces chemokine responses that may be associated with mucosal inflammation. To determine whether epithelial cells can contribute to BFT-induced inflammation, we assessed the expression of cyclooxygenase (COX)-2 in BFT-stimulated human intestinal epithelial cells. Human intestinal epithelial cell lines, HT-29 and Caco-2, were incubated with purified BFT. COX-2 mRNA and protein expression were measured by quantitative RT-PCR and Western blot analysis, respectively. BFT increased expression of COX-2, not that of COX-1, in human intestinal epithelial cell lines. Up-regulated COX-2 expression was paralleled by increased prostaglandin E2 (PGE2) production measured by the radioimmunoassay. PGE2 was predominantly secreted from the basolateral surface of BFT-treated epithelial cells, whereas lactate dehydrogenase was released predominantly from the apical surface. Moreover, the COX-2 expression and PGE2 production were significantly suppressed when NF-kappaB activity was inhibited. The basolateral secretion of PGE2 by up-regulated COX-2 in the BFT-stimulated colon epithelial cells seems to contribute to the inflammatory response in the underlying intestinal mucosa.
