J Korean Soc Microbiol.  1999 Oct;34(5):479-489.

Expression of Cyclooxygenase - 2 in Intestinal Epithelial Cells in Response to Invasive Bacterial Infection and its Role of Epithelial Cell Apoptosis

Abstract

Invasion of enteric bacteria, such as Salmonella and invasive E. coli, into intestinal epithelial cells induces proinflammatory gene responses and finally epithelial cell apoptosis. In this study, we asked whether invasive bacterial infection of human intestinal epithelial cells could upregulate cyclooxygenase-2 (COX-2) gene expression and whether increased COX-2 expression could influence intestinal epithelial cell apoptosis. Expression of COX-2 mRNA and prostaglandin (PG) E production were upregulated in HT-29 colon epithelial cells which were infected with S. dublin or invasive E. coli, as examined by quantitative RT-PCR and radioimmunoassay. Inhibition of COX-2 expression and PGE2 production using NS-398, a specific COX-2 inhibitor, showed a significant increase af epithelial cell apoptosis and caspase-3 activation in HT-29 cells infected with invasive bacteria. However, the addition of valerylsalicylate, a specific COX-1 inhibitor, did not change apoptosis in S. dublin-infected HT-29 cells. These results suggest that upregulated COX-2 expression and PGE2 production in response to invasive bacterial infection could contribute to host defense by inhibiting apoptosis of intestinal epithelial cells.

Keyword

Apoptosis; Cyclooxygenase-2; Intestinal epithelial cells; Invasive bacteria; Prostaglandin E2; Quantitative RT-PCR

MeSH Terms

Apoptosis*
Bacteria
Bacterial Infections*
Caspase 3
Colon
Cyclooxygenase 2
Dinoprostone
Enterobacteriaceae
Epithelial Cells*
Gene Expression
HT29 Cells
Humans
Prostaglandin-Endoperoxide Synthases*
Radioimmunoassay
RNA, Messenger
Salmonella
Caspase 3
Cyclooxygenase 2
Dinoprostone
Prostaglandin-Endoperoxide Synthases
RNA, Messenger
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