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Article: Essential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylori
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TitleEssential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylori
 
AuthorsWong, BLW2
Zhu, SL2 3
Huang, XR2
Juan, M2 1
Xia, HHX2
Bucala, R4
Wong, BCY2
Lan, HY2
 
Issue Date2009
 
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
 
CitationAmerican Journal Of Pathology, 2009, v. 174 n. 4, p. 1319-1328 [How to Cite?]
DOI: http://dx.doi.org/10.2353/ajpath.2009.080708
 
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.
 
ISSN0002-9440
2013 Impact Factor: 4.602
 
DOIhttp://dx.doi.org/10.2353/ajpath.2009.080708
 
ISI Accession Number IDWOS:000264657800018
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.).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWong, BLW
 
dc.contributor.authorZhu, SL
 
dc.contributor.authorHuang, XR
 
dc.contributor.authorJuan, M
 
dc.contributor.authorXia, HHX
 
dc.contributor.authorBucala, R
 
dc.contributor.authorWong, BCY
 
dc.contributor.authorLan, HY
 
dc.date.accessioned2010-05-31T03:46:19Z
 
dc.date.available2010-05-31T03:46:19Z
 
dc.date.issued2009
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationAmerican Journal Of Pathology, 2009, v. 174 n. 4, p. 1319-1328 [How to Cite?]
DOI: http://dx.doi.org/10.2353/ajpath.2009.080708
 
dc.identifier.doihttp://dx.doi.org/10.2353/ajpath.2009.080708
 
dc.identifier.epage1328
 
dc.identifier.hkuros159001
 
dc.identifier.isiWOS:000264657800018
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.).

 
dc.identifier.issn0002-9440
2013 Impact Factor: 4.602
 
dc.identifier.issue4
 
dc.identifier.openurl
 
dc.identifier.pmid19286569
 
dc.identifier.scopuseid_2-s2.0-65349155773
 
dc.identifier.spage1319
 
dc.identifier.urihttp://hdl.handle.net/10722/59256
 
dc.identifier.volume174
 
dc.languageeng
 
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAmerican Journal of Pathology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshAntigens, Bacterial
 
dc.subject.meshAntigens, Differentiation, B-Lymphocyte - immunology - metabolism
 
dc.subject.meshCell Differentiation - immunology
 
dc.subject.meshFlow Cytometry
 
dc.subject.meshGastritis - immunology - microbiology
 
dc.subject.meshHelicobacter Infections - immunology
 
dc.subject.meshHelicobacter pylori - immunology
 
dc.subject.meshHistocompatibility Antigens Class II - immunology - metabolism
 
dc.subject.meshHypersensitivity, Delayed
 
dc.subject.meshImmunohistochemistry
 
dc.subject.meshIntercellular Adhesion Molecule-1 - immunology - metabolism
 
dc.subject.meshIntramolecular Oxidoreductases - immunology - metabolism
 
dc.subject.meshMacrophage Migration-Inhibitory Factors - immunology - metabolism
 
dc.subject.meshMice
 
dc.subject.meshMice, Knockout
 
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction
 
dc.subject.meshTh1 Cells - cytology - immunology
 
dc.subject.meshTumor Necrosis Factor-alpha - immunology - metabolism
 
dc.titleEssential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylori
 
dc.typeArticle
 
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<contributor.author>Xia, HHX</contributor.author>
<contributor.author>Bucala, R</contributor.author>
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<subject.mesh>Animals</subject.mesh>
<subject.mesh>Antigens, Bacterial</subject.mesh>
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Author Affiliations
  1. Guangdong Provincial People's Hospital
  2. The University of Hong Kong
  3. Sun Yat-Sen University
  4. Yale University School of Medicine