File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Essential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylori

TitleEssential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylori
Authors
Issue Date2009
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal Of Pathology, 2009, v. 174 n. 4, p. 1319-1328 How to Cite?
AbstractMacrophage migration inhibitory factor (MIF) is an upstream regulator of immune and inflammatory responses; however, its role in Helicobacter pylori (HP)-associated gastritis remains unknown. We infected MIF knockout (KO) and wild-type mice with SS1 HP and found that 2 weeks after infection, MIF and its receptor CD74 were markedly up-regulated in wild-type mice. This up-regulation preceded the up-regulation of both tumor necrosis factor-α and intercellular adhesion molecule-1, as well as the development of moderate gastritis at 8 weeks, as determined by a significant infiltration of neutrophils, T cells, and macrophages. In contrast, KO mice were protected against HP-induced gastritis by preventing the up-regulation of CD74 and Th1-mediated immune injury, including a reduction in the Th1 transcriptional factor T-bet and the expression of interferon-γ. Additionally, inhibition of skin delayed type hypersensitivity reactions to HP antigens in KO mice also suggested a critical role for MIF in cell-mediated injury. A regulatory role for MIF in Th1-immune responses was further demonstrated by the finding that antigen- primed CD4+ T cells lacking MIF failed to differentiate into the Th1 phenotype; these cells were instead promoted to Th2 differentiation after challenge with HP antigen in vitro. Results from this study indicated that inhibition of HP-induced innate immune responses and Th1-mediated immune injury may be the key mechanisms by which KO mice failed to develop gastritis after HP infection. Copyright © American Society for Investigative Pathology.
Persistent Identifierhttp://hdl.handle.net/10722/59256
ISSN
2015 Impact Factor: 4.206
2015 SCImago Journal Rankings: 2.653
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant CouncilRGC GRF 759206
NIH
Funding Information:

Supported by grants from Hong Kong Research Grant Council (RGC GRF 759206) and the NIH (to R.B.).

References

 

DC FieldValueLanguage
dc.contributor.authorWong, BLWen_HK
dc.contributor.authorZhu, SLen_HK
dc.contributor.authorHuang, XRen_HK
dc.contributor.authorJuan, Men_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorBucala, Ren_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorLan, HYen_HK
dc.date.accessioned2010-05-31T03:46:19Z-
dc.date.available2010-05-31T03:46:19Z-
dc.date.issued2009en_HK
dc.identifier.citationAmerican Journal Of Pathology, 2009, v. 174 n. 4, p. 1319-1328en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59256-
dc.description.abstractMacrophage migration inhibitory factor (MIF) is an upstream regulator of immune and inflammatory responses; however, its role in Helicobacter pylori (HP)-associated gastritis remains unknown. We infected MIF knockout (KO) and wild-type mice with SS1 HP and found that 2 weeks after infection, MIF and its receptor CD74 were markedly up-regulated in wild-type mice. This up-regulation preceded the up-regulation of both tumor necrosis factor-α and intercellular adhesion molecule-1, as well as the development of moderate gastritis at 8 weeks, as determined by a significant infiltration of neutrophils, T cells, and macrophages. In contrast, KO mice were protected against HP-induced gastritis by preventing the up-regulation of CD74 and Th1-mediated immune injury, including a reduction in the Th1 transcriptional factor T-bet and the expression of interferon-γ. Additionally, inhibition of skin delayed type hypersensitivity reactions to HP antigens in KO mice also suggested a critical role for MIF in cell-mediated injury. A regulatory role for MIF in Th1-immune responses was further demonstrated by the finding that antigen- primed CD4+ T cells lacking MIF failed to differentiate into the Th1 phenotype; these cells were instead promoted to Th2 differentiation after challenge with HP antigen in vitro. Results from this study indicated that inhibition of HP-induced innate immune responses and Th1-mediated immune injury may be the key mechanisms by which KO mice failed to develop gastritis after HP infection. Copyright © American Society for Investigative Pathology.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.relation.ispartofAmerican Journal of Pathologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntigens, Bacterialen_HK
dc.subject.meshAntigens, Differentiation, B-Lymphocyte - immunology - metabolismen_HK
dc.subject.meshCell Differentiation - immunologyen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshGastritis - immunology - microbiologyen_HK
dc.subject.meshHelicobacter Infections - immunologyen_HK
dc.subject.meshHelicobacter pylori - immunologyen_HK
dc.subject.meshHistocompatibility Antigens Class II - immunology - metabolismen_HK
dc.subject.meshHypersensitivity, Delayeden_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshIntercellular Adhesion Molecule-1 - immunology - metabolismen_HK
dc.subject.meshIntramolecular Oxidoreductases - immunology - metabolismen_HK
dc.subject.meshMacrophage Migration-Inhibitory Factors - immunology - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshTh1 Cells - cytology - immunologyen_HK
dc.subject.meshTumor Necrosis Factor-alpha - immunology - metabolismen_HK
dc.titleEssential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylorien_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9440&volume=174&issue=4&spage=1319&epage=28&date=2009&atitle=Essential+role+for+macrophage+migration+inhibitory+factor+in+gastritis+induced+by+Helicobacter+pylorien_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2353/ajpath.2009.080708en_HK
dc.identifier.pmid19286569en_HK
dc.identifier.scopuseid_2-s2.0-65349155773en_HK
dc.identifier.hkuros159001en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65349155773&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume174en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1319en_HK
dc.identifier.epage1328en_HK
dc.identifier.isiWOS:000264657800018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, BLW=24171921500en_HK
dc.identifier.scopusauthoridZhu, SL=7404391208en_HK
dc.identifier.scopusauthoridHuang, XR=7410248090en_HK
dc.identifier.scopusauthoridJuan, M=26532933800en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridBucala, R=7102379822en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridLan, HY=7102710832en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats