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Conference Paper: Effects of cyclooxygenase-1 and -2 gene disruption onhelicobacter pylori-induced inflammation, apoptosisand proliferation

TitleEffects of cyclooxygenase-1 and -2 gene disruption onhelicobacter pylori-induced inflammation, apoptosisand proliferation
Authors
Issue Date2004
PublisherBlackwell Publishing Asia.
Citation
Asian-Pacific Digestive Week 2004, Beijing, China, 4-7 October 2004. In Journal of Gastroenterology and Hepatology, 2004, v. 19 n. S5, p. A299 Abstract no. F1-11 How to Cite?
AbstractObjectives To investigate the effects of COX-1 and COX-2 dis-ruption on H. pylori (Hp)-induced gastric inflammation, apoptosisand proliferation.Methods Hp strain TN2 was inoculated into the stomachs of COX-1 and COX-2 deficient homozygous (COX-1-/-, COX-2-/-) and con-geneic wild-type (WT) mice. Mice were sacrificed 24 wks later (n =8–10 mice/group). WT, COX-1-/- and COX-2-/- mice without Hpinoculation were used as controls.The density of Hp colonization, theseverity of chronic gastric inflammation, apoptosis and proliferationof gastric epithelial cells, TNF-a and PGE2were determined.Results There was no significant difference in the density of Hpcolonization between WT and COX-/- mice. Hp-induced gastritis wasmarkedly more severe in both COX-1-/- and COX-2-/- mice. Hp infec-tion increased apoptosis in WT (4.7-fold) and COX-1-/- (4.8-fold)mice, compared with their uninfected controls. Apoptosis was furtherincreased in Hp infected COX-2-/- mice compared with Hp infectedWT and COX-1-/- mice although the difference was not statisticallysignificance. Cell proliferation was increased in WT (2.3-fold) andCOX-1-/- (2.4-fold) mice, but not in COX-2-/- mice in the presenceof Hp infection. Hp infection increased expression of gastric mucosalTNF-a mRNA (4.4-fold) in WT mice, and further increased TNF-amRNA expression in COX-1-/- (1.8-fold vs.WT) and COX-2-/- (2.0-fold vs. WT) mice. Hp infection increased gastric PGE2level in WT(1.6-fold) and COX-2-/- (1.4-fold) mice. PGE2was detected at verylow levels in COX-1-/- mice with or without Hp infection.Conclusion In a 24-wk Hp colonization study model, COX-1 andCOX-2 deficiency enhances Hp-induced gastritis, probably via TNF-a expression, but has no significant effect on Hp-induced apoptosis.Deficiency of COX-2, but not COX-1, inhibits Hp-induced cell proliferation.
Persistent Identifierhttp://hdl.handle.net/10722/101948
ISSN
2015 Impact Factor: 3.322
2015 SCImago Journal Rankings: 1.190

 

DC FieldValueLanguage
dc.contributor.authorLi, Gen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorChen, MHen_HK
dc.contributor.authorChan, OOen_HK
dc.contributor.authorCho, CHen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorBerg, Den_HK
dc.contributor.authorFeng, Zen_HK
dc.contributor.authorLangenbach, Ren_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-25T20:10:56Z-
dc.date.available2010-09-25T20:10:56Z-
dc.date.issued2004en_HK
dc.identifier.citationAsian-Pacific Digestive Week 2004, Beijing, China, 4-7 October 2004. In Journal of Gastroenterology and Hepatology, 2004, v. 19 n. S5, p. A299 Abstract no. F1-11en_HK
dc.identifier.issn0815-9319en_HK
dc.identifier.urihttp://hdl.handle.net/10722/101948-
dc.description.abstractObjectives To investigate the effects of COX-1 and COX-2 dis-ruption on H. pylori (Hp)-induced gastric inflammation, apoptosisand proliferation.Methods Hp strain TN2 was inoculated into the stomachs of COX-1 and COX-2 deficient homozygous (COX-1-/-, COX-2-/-) and con-geneic wild-type (WT) mice. Mice were sacrificed 24 wks later (n =8–10 mice/group). WT, COX-1-/- and COX-2-/- mice without Hpinoculation were used as controls.The density of Hp colonization, theseverity of chronic gastric inflammation, apoptosis and proliferationof gastric epithelial cells, TNF-a and PGE2were determined.Results There was no significant difference in the density of Hpcolonization between WT and COX-/- mice. Hp-induced gastritis wasmarkedly more severe in both COX-1-/- and COX-2-/- mice. Hp infec-tion increased apoptosis in WT (4.7-fold) and COX-1-/- (4.8-fold)mice, compared with their uninfected controls. Apoptosis was furtherincreased in Hp infected COX-2-/- mice compared with Hp infectedWT and COX-1-/- mice although the difference was not statisticallysignificance. Cell proliferation was increased in WT (2.3-fold) andCOX-1-/- (2.4-fold) mice, but not in COX-2-/- mice in the presenceof Hp infection. Hp infection increased expression of gastric mucosalTNF-a mRNA (4.4-fold) in WT mice, and further increased TNF-amRNA expression in COX-1-/- (1.8-fold vs.WT) and COX-2-/- (2.0-fold vs. WT) mice. Hp infection increased gastric PGE2level in WT(1.6-fold) and COX-2-/- (1.4-fold) mice. PGE2was detected at verylow levels in COX-1-/- mice with or without Hp infection.Conclusion In a 24-wk Hp colonization study model, COX-1 andCOX-2 deficiency enhances Hp-induced gastritis, probably via TNF-a expression, but has no significant effect on Hp-induced apoptosis.Deficiency of COX-2, but not COX-1, inhibits Hp-induced cell proliferation.-
dc.languageengen_HK
dc.publisherBlackwell Publishing Asia.en_HK
dc.relation.ispartofJournal of Gastroenterology and Hepatologyen_HK
dc.titleEffects of cyclooxygenase-1 and -2 gene disruption onhelicobacter pylori-induced inflammation, apoptosisand proliferationen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0815-9319&volume=19&issue=Suppl.&spage=A299&epage=&date=2004&atitle=Effects+of+Cyclooxygenase-1+and+-2+Gene+Disruption+on+Helicobacter+pylori-Induced+Inflammation,+Apoptosis+and+Proliferationen_HK
dc.identifier.emailXia, HHX: xiaharry@hotmail.comen_HK
dc.identifier.emailChan, OO: aoochan@hku.hken_HK
dc.identifier.emailCho, CH: chcho@hkusua.hku.hken_HK
dc.identifier.emailLam, SK: deanmed@hku.hken_HK
dc.identifier.emailFeng, Z: zhfeng@hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1440-1746.2004.t01-1-03624.x-
dc.identifier.hkuros96322en_HK
dc.identifier.volume19en_HK
dc.identifier.issueS5en_HK
dc.identifier.spage299en_HK

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