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Toxicologic Pathology
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Articles

Differential Expression of COX-1 and COX-2 in the Gastrointestinal Tract of the Rat

Richard Haworth, Keli Oakley, Nicola McCormack and Andrew Pilling*

Department of Pathology, Safety Assessment, GlaxoSmithKline Research and Development Ltd., Ware, Herts SG12 0DP, United Kingdom

Correspondence: Address correspondence to: Richard Haworth, Department of Pathology, Safety Assessment, GlaxoSmithKline Research and Development Ltd, Park Road, Ware, Herts SG12 0DP, United Kingdom; e-mail:richard.i.haworth{at}gsk.com

The aim of this study was to use immunohistochemistry with morphometry to investigate COX-1 and COX-2 expression in the normal rat gastrointestinal (GI) tract and examine if sites of ulceration previously observed with long-term COX-2 inhibitor administration in mice correlate with differential COX-1/COX-2 expression. COX-2 positive cells were observed predominantly in the apical lamina propria of intestinal villi with fewer cells in the mucosal epithelium. The highest level of COX-2 expression was observed at the ileocaecal junction (ICJ). COX-2 expression was also present in parasympathetic ganglia of the submucosa and muscularis. In the stomach, the highest grade of COX-2 expression was observed in the apical lamina propria of the fundus adjacent to the junctional ridge. In contrast, COX-1 positive cells within the lamina propria were evenly distributed along the GI tract but were present in higher numbers than COX-2 positive cells. The mean level of COX-1 expression at the ICJ was not significantly different from the ileum and caecum. Evidence that the highest level of COX-2 expression in normal rats is located on the ileal side of the ICJ provides the first mechanism to explain spontaneous ulceration and perforation of the distal ileum in COX-2–/– animals.

Key Words: Rat • COX-1 • COX-2 • immunohistochemistry • NSAID • intestine • ileocaecal junction

Abbreviations: COX, cyclooxygenase • GI, gastrointestinal • ICJ, ileocaecal junction • LPS, lipopolysaccharide • NSAID, nonsteroidal antiinflammatory drug • PGE, prostaglandin-E • PGI, prostaglandin-I

Toxicologic Pathology, Vol. 33, No. 2, 239-245 (2005)
DOI: 10.1080/01926230590906512
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