title: Induction of cyclooxygenase-2 in mesothelial cells in peritonitis caused by perforated ulcers--an immunohistochemical study in humans.
abstract: 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 cyclooxygenase (COX)-2 knockout mice die partly as a result of peritonitis.
  
  
  OBJECTIVE
  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.
authors.affiliation: Third Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Tatsuguchi
authors.forename: C
authors.initials: C
authors.lastname: Sakamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Fukuda
authors.forename: K
authors.initials: K
authors.lastname: Wada
authors.forename: T
authors.initials: T
authors.lastname: Akamatsu
authors.forename: T
authors.initials: T
authors.lastname: Tsukui
authors.forename: K
authors.initials: K
authors.lastname: Miyake
authors.forename: S
authors.initials: S
authors.lastname: Futagami
authors.forename: T
authors.initials: T
authors.lastname: Kishida
authors.forename: N
authors.initials: N
authors.lastname: Yamanaka
authors.forename: M
authors.initials: M
authors.lastname: Kobayashi
mesh_terms: D000328:Adult; D000368:Aged; D051546:Cyclooxygenase 2; D004790:Enzyme Induction; D004848:Epithelium / Q000201:enzymology; D005260:Female; D005347:Fibroblasts; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation; D007416:Intestinal Perforation / Q000150:complications*; D007527:Isoenzymes / Q000378:metabolism*; D008264:Macrophages; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D010437:Peptic Ulcer / Q000150:complications*; D010538:Peritonitis / Q000201:enzymology / Q000209:etiology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*
chemical_list: D007527:Isoenzymes; D008565:Membrane Proteins; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases