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Article: Effects of cyclooxygenase-1 and -2 gene disruption on Helicobacter pylori-induced gastric inflammation

TitleEffects of cyclooxygenase-1 and -2 gene disruption on Helicobacter pylori-induced gastric inflammation
Authors
KeywordsCyclooxygenase 1 - deficiency - genetics - physiology
Cyclooxygenase 2 - deficiency - genetics - physiology
Gastric Mucosa - immunology - microbiology - pathology
Gastritis - enzymology - immunology - microbiology - pathology
Helicobacter Infections - enzymology - immunology - microbiology - pathology
Issue Date2006
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2006, v. 193 n. 7, p. 1037-1046 How to Cite?
AbstractBackground. Cyclooxygenases (COXs) play important roles in inflammation and carcinogenesis. The present study aimed to determine the effects of COX-1 and COX-2 gene disruption on Helicobacter pylori-induced gastric inflammation. Methods. Wild-type (WT), COX-1 and COX-2 heterozygous (COX-1 +/- and COX-2 +/-), and homozygous COX-deficient (COX-1 -/- and COX-2 -/-) mice were inoculated with H. pylori strain TN2 and killed after 24 weeks of infection. Uninfected WT and COX-deficient mice were used as controls. Levels of gastric mucosal inflammation, epithelial cell proliferation and apoptosis, and cytokine expression were determined. Results. COX deficiency facilitated H. pylori-induced gastritis. In the presence of H. pylori infection, apoptosis was increased in both WT and COX-deficient mice, whereas cell proliferation was increased in WT and COX-1-deficient, but not in COX-2-deficient, mice. Tumor necrosis factor (TNF)-α and interleukin-10 mRNA expression was elevated in H. pylori-infected mice, but only TNF-α mRNA expression was further increased by COX deficiency. Prostaglandin E 2 levels were increased in infected WT and COX-2-deficient mice but were at very low levels in infected COX-1-deficient mice. Leukotriene (LT) B 4 and LTC 4 levels were increased to a similar extent in infected WT and COX-deficient mice. Conclusions. COX deficiency enhances H. pylori-induced gastritis, probably via TNF-α expression. COX-2, but not COX-1, deficiency suppresses H. pylori-induced cell proliferation. © 2006 by the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/45019
ISSN
2015 Impact Factor: 6.344
2015 SCImago Journal Rankings: 4.000
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, GQen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorChen, MHen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorWang, JDen_HK
dc.contributor.authorPeng, JZen_HK
dc.contributor.authorChan, AOOen_HK
dc.contributor.authorCho, CHen_HK
dc.contributor.authorSo, HLen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorHu, PJen_HK
dc.contributor.authorLiang, YJen_HK
dc.contributor.authorLin, HLen_HK
dc.contributor.authorBerg, DEen_HK
dc.contributor.authorFeng, ZHen_HK
dc.contributor.authorLangenbach, Ren_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2007-10-30T06:15:45Z-
dc.date.available2007-10-30T06:15:45Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2006, v. 193 n. 7, p. 1037-1046en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/45019-
dc.description.abstractBackground. Cyclooxygenases (COXs) play important roles in inflammation and carcinogenesis. The present study aimed to determine the effects of COX-1 and COX-2 gene disruption on Helicobacter pylori-induced gastric inflammation. Methods. Wild-type (WT), COX-1 and COX-2 heterozygous (COX-1 +/- and COX-2 +/-), and homozygous COX-deficient (COX-1 -/- and COX-2 -/-) mice were inoculated with H. pylori strain TN2 and killed after 24 weeks of infection. Uninfected WT and COX-deficient mice were used as controls. Levels of gastric mucosal inflammation, epithelial cell proliferation and apoptosis, and cytokine expression were determined. Results. COX deficiency facilitated H. pylori-induced gastritis. In the presence of H. pylori infection, apoptosis was increased in both WT and COX-deficient mice, whereas cell proliferation was increased in WT and COX-1-deficient, but not in COX-2-deficient, mice. Tumor necrosis factor (TNF)-α and interleukin-10 mRNA expression was elevated in H. pylori-infected mice, but only TNF-α mRNA expression was further increased by COX deficiency. Prostaglandin E 2 levels were increased in infected WT and COX-2-deficient mice but were at very low levels in infected COX-1-deficient mice. Leukotriene (LT) B 4 and LTC 4 levels were increased to a similar extent in infected WT and COX-deficient mice. Conclusions. COX deficiency enhances H. pylori-induced gastritis, probably via TNF-α expression. COX-2, but not COX-1, deficiency suppresses H. pylori-induced cell proliferation. © 2006 by the Infectious Diseases Society of America. All rights reserved.en_HK
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dc.format.mimetypeapplication/pdf-
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dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.orgen_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.rightsJournal of Infectious Diseases. Copyright © University of Chicago Press.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCyclooxygenase 1 - deficiency - genetics - physiologyen_HK
dc.subjectCyclooxygenase 2 - deficiency - genetics - physiologyen_HK
dc.subjectGastric Mucosa - immunology - microbiology - pathologyen_HK
dc.subjectGastritis - enzymology - immunology - microbiology - pathologyen_HK
dc.subjectHelicobacter Infections - enzymology - immunology - microbiology - pathologyen_HK
dc.titleEffects of cyclooxygenase-1 and -2 gene disruption on Helicobacter pylori-induced gastric inflammationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1899&volume=193&issue=7&spage=1037&epage=1046&date=2006&atitle=Effects+of+cyclooxygenase-1+and+-2+gene+disruption+on+Helicobacter+pylori+-+induced+gastric+inflammationen_HK
dc.identifier.emailWang, JD: jidewang@gmail.comen_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityWang, JD=rp00491en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1086/500984en_HK
dc.identifier.pmid16518767-
dc.identifier.scopuseid_2-s2.0-33645375383en_HK
dc.identifier.hkuros116884-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645375383&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume193en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1037en_HK
dc.identifier.epage1046en_HK
dc.identifier.isiWOS:000235777000018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, GQ=8692805500en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridChen, MH=8642044500en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridWang, JD=35309087500en_HK
dc.identifier.scopusauthoridPeng, JZ=12796973500en_HK
dc.identifier.scopusauthoridChan, AOO=7403167965en_HK
dc.identifier.scopusauthoridCho, CH=7403100461en_HK
dc.identifier.scopusauthoridSo, HL=7102300031en_HK
dc.identifier.scopusauthoridLam, SK=55424391900en_HK
dc.identifier.scopusauthoridHu, PJ=7201989582en_HK
dc.identifier.scopusauthoridLiang, YJ=12804573800en_HK
dc.identifier.scopusauthoridLin, HL=8950219500en_HK
dc.identifier.scopusauthoridBerg, DE=7202401139en_HK
dc.identifier.scopusauthoridFeng, ZH=7403442974en_HK
dc.identifier.scopusauthoridLangenbach, R=35444992800en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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