Induction of cyclooxygenase-2 in mesothelial cells in peritonitis caused by perforated ulcers – an immunohistochemical study in humans

1365-2036

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background: Increasing evidence suggests that mesothelial cells contribute to the control of inflammation in the peritoneal cavity by secreting prostaglandins. A study has shown that cyclo-oxygenase (COX)-2 knockout mice die partly as a result of peritonitis. Aim: To investigate the expression and location of COX in peritonitis associated with peptic ulcer perforation. Methods: Gastric and duodenal tissues were collected intraoperatively from nine and four patients, respectively, and immunohistochemical staining for COX-1 and COX-2 was performed. Results: Histologically, all patients had severe peritonitis around the perforation sites, into which many inflammatory cells and fibroblasts had infiltrated, and reactive mesothelial cells exhibited hyperplastic change. The COX-1 protein was not detected, whereas COX-2 was abundant in reactive mesothelial cells near the perforation site and disappeared away from the site. Macrophages and fibroblasts around the perforation site also revealed immunostaining for COX-2. Conclusions: Our results showed that COX-2 protein is induced in mesothelial cells, as well as in macrophages and fibroblasts, in inflamed peritoneal tissues associated with peptic ulcer perforation, suggesting involvement of COX-2 in tissue repair.

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