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 inJournal of bacteriology and virology Vol. 32; no. 2; pp. 147 - 157
Main Authors 김정목, Jung Mogg Kim, 강신재, Shin Jae Kang, 조수진, Soo Jin Cho, 정훈용, Hwoon Yong Jung, 오유경, Yu Kyoung Oh, 김영전, Young Jeon Kim
Format Journal Article
LanguageKorean
Published 대한바이러스학회 2002
대한미생물학회
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ISSN1598-2467
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.
Bibliography:The Korean Society of Virology
KISTI1.1003/JNL.JAKO200217153869403
G704-000075.2002.32.2.001
ISSN:1598-2467
2093-0429