Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 184, Issue 5, Pages 648-652Publisher
UNIV CHICAGO PRESS
DOI: 10.1086/322799
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Funding
- FIC NIH HHS [5 D43 TW00909] Funding Source: Medline
- NIAID NIH HHS [AI-01573] Funding Source: Medline
- NIDDK NIH HHS [DK-55753, DK-33165, DK-52574] Funding Source: Medline
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Cyclooxygenase (Cox)-2 expression and inhibition were investigated in a rabbit ileal loop model of Clostridium difficile colitis and diarrhea. Intestinal tissue stimulated with C. difficile toxin A showed up-regulation of Cox-2 expression in lamina propria macrophages and elevated prostaglandin levels. Toxin A-stimulated loops exhibited severe inflammation and increased secretory volume. Celecoxib, a specific Cox-2 inhibitor, significantly reduced toxin A-induced prostaglandin production. Furthermore, celecoxib (greater than or equal to0.02 mg/mL) blocked both histologic damage (mean histologic grade, 1.25 vs. 3.44 in rabbits receiving toxin A alone; P < .0005) and secretion (volume: length ratio, 0.18 vs. 0.72 in those receiving toxin A alone; P = .002) in toxin A-stimulated loops in a dose-related manner. Thus, toxin A induced expression of Cox-2 in the host, and prostaglandins produced through Cox-2 were involved in the mediation of the increased secretion of electrolytes and water and the inflammatory response induced by toxin A.
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