AIMS: To test the hypothesis that both COX-1 and COX-2 expression in human gastric mucosa is up-regulated in the presence of inflammation as seen in patients with gastritis and gastric ulcers. METHODS AND RESULTS: We performed immunohistochemistry using COX-1 and COX-2 monoclonal antibodies on gastric biopsies from 59 patients with normal mucosa, gastritis and gastric ulcers. Expression of COX-1 and COX-2 was quantified using an intensity proportion scoring system. Expression of COX-1 was primarily seen in the lamina propria mononuclear cells with some expression in deep gastric glands in the ulcer group. Expression of COX-2 was primarily seen in the deep gastric glands with focal expression in the lamina propria mononuclear cells. We found a stepwise increase in the expression of both COX-1 and COX-2 as mucosal damage progressed from normal to gastritis to gastric ulcer. CONCLUSIONS: We conclude that both COX-1 and COX-2 expression in the gastric mucosa are increased in the setting of gastritis and gastric ulceration. Although this increased expression may be due, at least in part, to an increase in inflammatory cell numbers, this study raises the possibility that both COX-1 and COX-2 are inducible, contrary to the traditionally held view of only COX-2 being inducible.
AIMS: To test the hypothesis that both COX-1 and COX-2 expression in human gastric mucosa is up-regulated in the presence of inflammation as seen in patients with gastritis and gastric ulcers. METHODS AND RESULTS: We performed immunohistochemistry using COX-1 and COX-2 monoclonal antibodies on gastric biopsies from 59 patients with normal mucosa, gastritis and gastric ulcers. Expression of COX-1 and COX-2 was quantified using an intensity proportion scoring system. Expression of COX-1 was primarily seen in the lamina propria mononuclear cells with some expression in deep gastric glands in the ulcer group. Expression of COX-2 was primarily seen in the deep gastric glands with focal expression in the lamina propria mononuclear cells. We found a stepwise increase in the expression of both COX-1 and COX-2 as mucosal damage progressed from normal to gastritis to gastric ulcer. CONCLUSIONS: We conclude that both COX-1 and COX-2 expression in the gastric mucosa are increased in the setting of gastritis and gastric ulceration. Although this increased expression may be due, at least in part, to an increase in inflammatory cell numbers, this study raises the possibility that both COX-1 and COX-2 are inducible, contrary to the traditionally held view of only COX-2 being inducible.
Authors: A Dudley; J Thomason; S Fritz; J Grady; J Stokes; R Wills; L Pinchuk; A Mackin; K Lunsford Journal: J Vet Intern Med Date: 2012-12-26 Impact factor: 3.333
Authors: J C Desai; T Goo; M Fukata; S Sanyal; A Dikman; K Miller; L Cohen; A Brooks; Q Wang; M T Abreu; J Aisenberg Journal: Aliment Pharmacol Ther Date: 2009-03-19 Impact factor: 8.171
Authors: Pradeep Bhandari; Adrian C Bateman; Raj L Mehta; Bernard Sf Stacey; Penny Johnson; Ian A Cree; Federica Di Nicolantonio; Praful Patel Journal: BMC Cancer Date: 2006-05-19 Impact factor: 4.430
Authors: Irina Amorim; Marian A Taulescu; Andreia Ferreira; Alexandra Rêma; Celso A Reis; Augusto M Faustino; Cornel Cătoi; Fátima Gärtner Journal: Diagn Pathol Date: 2014-09-18 Impact factor: 2.644