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

Background: Increasing evidence mesothelial cells contribute to the control of inflammation in the peritoneal cavity by secreting prostaglandins. A st udy has shown that cyclooxygenase (COX)-2 knockout mice die partly as a res ult of peritonitis. Aim: To investigate the expression and location of COX in peritonitis assoc iated 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 per foration sites, into which many inflammatory cells and fibroblasts had infi ltrated, and reactive mesothelial cells exhibited hyperplastic change. The COX-1 protein was not detected, whereas COX-2 was abundant in reactive meso thelial cells near the perforation site and disappeared away from the site. Macrophages and fibroblasts around the perforation site also revealed immu nostaining for COX-2. Conclusions: Our results showed that COX-2 protein is induced in mesothelia l 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.