Bacteroides fragilis 장독소 자극에 의한 인체 장상피세포에서의 Cyclooxygenase-2 발현
A ${\sim}20\;kDa$ heat-labile toxin (EFT) 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 BF...
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Published in | Journal of bacteriology and virology Vol. 32; no. 2; pp. 147 - 157 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | Korean |
Published |
대한바이러스학회
2002
대한미생물학회 |
Subjects | |
Online Access | Get full text |
ISSN | 1598-2467 2093-0429 |
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Summary: | A ${\sim}20\;kDa$ heat-labile toxin (EFT) 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 $E_2\;(PGE_2)$ production measured by the radioimmunoassay. $PGE_2$ 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 $PGE_2$ production were significantly suppressed when NF-${\kappa}B$ activity was inhibited. The basolateral secretion of $PGE_2$ by up-regulated COX-2 in the BFT-stimulated colon epithelial cells seems to contribute to the inflammatory response in the underlying intestinal mucosa. |
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Bibliography: | The Korean Society of Virology KISTI1.1003/JNL.JAKO200217153869403 G704-000075.2002.32.2.001 |
ISSN: | 1598-2467 2093-0429 |