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Infection and Immunity, November 2003, p. 6234-6242, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6234-6242.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Role of Cyclooxygenase Enzymes in a Murine Model of Experimental Cholera

Deborah L. Gessell-Lee,1* Vsevolod L. Popov,2 Istvan Boldogh,1 Juan P. Olano,2 and Johnny W. Peterson1

Department of Microbiology and Immunology,1 Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555-06092

Received 3 April 2003/ Returned for modification 3 June 2003/ Accepted 11 August 2003

Nonsteroidal anti-inflammatory drugs (e.g., indomethacin) inhibit and reduce the fluid secretion responses elicited by cholera toxin (CT), but it has not been conclusively determined which cyclooxygenase (COX) isoform is involved in CT's action. This study evaluated the role of the COX enzymes and their arachidonic acid metabolites in experimental cholera. Swiss-Webster mice were dosed with celecoxib and rofecoxib and challenged with CT in ligated small intestinal loops, and intestinal segments from mice deficient in COX-1 and COX-2 were challenged with CT. The effects of CT on fluid accumulation, prostaglandin E2 production, mucosal tissue injury, and markers of oxidative stress were measured. Celecoxib and rofecoxib given at 160 µg per mouse inhibited CT-induced fluid accumulation by 48% and 31%, respectively, but there was no significant difference among cox-1-/- and cox-2-/- mice in response to CT compared to wild-type controls. CT elevated tissue levels of oxidized glutathione and lipid peroxides and elicited small intestinal tissue injury in two of five cox-1-/- and four of five cox-2-/- mice. A role for COX-2 in CT's mechanism of action has previously been suggested by the effectiveness of COX-2 inhibitors in reducing CT-induced fluid secretion, but CT challenge of COX-1 and COX-2 knockout mice did not corroborate the pharmacological data. The results of this study show that CT induced oxidative stress in COX-deficient mice and suggest a tissue-protective role for arachidonic acid metabolites in the small intestine against oxidative stress.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1070. Phone: (409) 772-3409. Fax: (409) 747-6869. E-mail: dlgessel{at}utmb.edu.

Editor: A. D. O'Brien

Infection and Immunity, November 2003, p. 6234-6242, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6234-6242.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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