Abstract:
BACKGROUND & AIMS:Although dextran sodium sulfate (DSS)-induced colitis is a commonly used model of colonic injury, the mechanism of this model is not understood. The aim of this study was to determine the contribution of prostaglandins to the mechanism of DSS-induced epithelial injury. METHODS:Mice were treated with 3% DSS in the drinking water for 5 days followed by water only (recovery). Tissue prostaglandin E2 (PGE2) levels were measured, proliferating cells per cecal crypt were determined by bromodeoxyuridine labeling, and the cellular localization of cyclooxygenase (COX)-1 and COX-2 was determined by immunohistochemistry. RESULTS:DSS decreased the number of proliferating epithelial cells per crypt by approximately 90% and decreased the height of cecal crypts by 40%. Administration of dimethyl PGE2 with DSS reversed the effect of DSS on proliferation but not its effect on crypt shortening. COX-1 was expressed in the crypt epithelium and lamina propria mononuclear cells; DSS treatment down-regulated COX-1 expression only in the epithelium. Dimethyl PGE2 reversed the effect of DSS on COX-1 expression. Recovery was associated with a return to normal COX-1 expression in the epithelium. COX-2 was expressed in lamina propria mononuclear cells. CONCLUSIONS:Epithelial cell proliferation in the presence of DSS contains a PGE2-sensitive component.
journal_name
Gastroenterologyjournal_title
Gastroenterologyauthors
Tessner TG,Cohn SM,Schloemann S,Stenson WFdoi
10.1016/s0016-5085(98)70259-8subject
Has Abstractpub_date
1998-10-01 00:00:00pages
874-82issue
4eissn
0016-5085issn
1528-0012pii
S0016508598003771journal_volume
115pub_type
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