Premium
Induction of cyclooxygenase‐2 in mesothelial cells in peritonitis caused by perforated ulcers – an immunohistochemical study in humans
Author(s) -
Tatsuguchi A.,
Sakamoto C.,
Fukuda Y.,
Wada K.,
Akamatsu T.,
Tsukui T.,
Miyake K.,
Futagami S.,
Kishida T.,
Yamanaka N.,
Kobayashi M.
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.014s1058.x
Subject(s) - medicine , mesothelial cell , peritonitis , immunohistochemistry , immunostaining , cyclooxygenase , perforation , pathology , peritoneum , inflammation , mesothelium , biology , enzyme , biochemistry , materials science , metallurgy , punching
Summary 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.