Article: Essential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylori
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- Publisher Website: 10.2353/ajpath.2009.080708
- Scopus: eid_2-s2.0-65349155773
- PMID: 19286569
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| Title | Essential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylori | ||||||
|---|---|---|---|---|---|---|---|
| Authors | Wong, BLW2 Zhu, SL2 3 Huang, XR2 Juan, M1 2 Xia, HHX2 Bucala, R4 Wong, BCY2 Lan, HY2 | ||||||
| Issue Date | 2009 | ||||||
| Publisher | American 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?] DOI: http://dx.doi.org/10.2353/ajpath.2009.080708 | ||||||
| Abstract | Macrophage 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. | ||||||
| ISSN | 0002-9440 2011 Impact Factor: 4.89 2011 SCImago Journal Rankings: 0.697 | ||||||
| DOI | http://dx.doi.org/10.2353/ajpath.2009.080708 | ||||||
| ISI Accession Number ID | WOS:000264657800018
Funding Information: Supported by grants from Hong Kong Research Grant Council (RGC GRF 759206) and the NIH (to R.B.). | ||||||
| References | References in Scopus |
| dc.contributor.author | Wong, BLW | ||||||
|---|---|---|---|---|---|---|---|
| dc.contributor.author | Zhu, SL | ||||||
| dc.contributor.author | Huang, XR | ||||||
| dc.contributor.author | Juan, M | ||||||
| dc.contributor.author | Xia, HHX | ||||||
| dc.contributor.author | Bucala, R | ||||||
| dc.contributor.author | Wong, BCY | ||||||
| dc.contributor.author | Lan, HY | ||||||
| dc.date.accessioned | 2010-05-31T03:46:19Z | ||||||
| dc.date.available | 2010-05-31T03:46:19Z | ||||||
| dc.date.issued | 2009 | ||||||
| dc.description.abstract | Macrophage 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.nature | Link_to_subscribed_fulltext | ||||||
| dc.identifier.citation | American 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.doi | http://dx.doi.org/10.2353/ajpath.2009.080708 | ||||||
| dc.identifier.epage | 1328 | ||||||
| dc.identifier.hkuros | 159001 | ||||||
| dc.identifier.isi | WOS:000264657800018
Funding Information: Supported by grants from Hong Kong Research Grant Council (RGC GRF 759206) and the NIH (to R.B.). | ||||||
| dc.identifier.issn | 0002-9440 2011 Impact Factor: 4.89 2011 SCImago Journal Rankings: 0.697 | ||||||
| dc.identifier.issue | 4 | ||||||
| dc.identifier.openurl | | ||||||
| dc.identifier.pmid | 19286569 | ||||||
| dc.identifier.scopus | eid_2-s2.0-65349155773 | ||||||
| dc.identifier.spage | 1319 | ||||||
| dc.identifier.uri | http://hdl.handle.net/10722/59256 | ||||||
| dc.identifier.volume | 174 | ||||||
| dc.language | eng | ||||||
| dc.publisher | American Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org | ||||||
| dc.publisher.place | United States | ||||||
| dc.relation.ispartof | American Journal of Pathology | ||||||
| dc.relation.references | References in Scopus | ||||||
| dc.subject.mesh | Animals | ||||||
| dc.subject.mesh | Antigens, Bacterial | ||||||
| dc.subject.mesh | Antigens, Differentiation, B-Lymphocyte - immunology - metabolism | ||||||
| dc.subject.mesh | Cell Differentiation - immunology | ||||||
| dc.subject.mesh | Flow Cytometry | ||||||
| dc.subject.mesh | Gastritis - immunology - microbiology | ||||||
| dc.subject.mesh | Helicobacter Infections - immunology | ||||||
| dc.subject.mesh | Helicobacter pylori - immunology | ||||||
| dc.subject.mesh | Histocompatibility Antigens Class II - immunology - metabolism | ||||||
| dc.subject.mesh | Hypersensitivity, Delayed | ||||||
| dc.subject.mesh | Immunohistochemistry | ||||||
| dc.subject.mesh | Intercellular Adhesion Molecule-1 - immunology - metabolism | ||||||
| dc.subject.mesh | Intramolecular Oxidoreductases - immunology - metabolism | ||||||
| dc.subject.mesh | Macrophage Migration-Inhibitory Factors - immunology - metabolism | ||||||
| dc.subject.mesh | Mice | ||||||
| dc.subject.mesh | Mice, Knockout | ||||||
| dc.subject.mesh | Reverse Transcriptase Polymerase Chain Reaction | ||||||
| dc.subject.mesh | Th1 Cells - cytology - immunology | ||||||
| dc.subject.mesh | Tumor Necrosis Factor-alpha - immunology - metabolism | ||||||
| dc.title | Essential role for macrophage migration inhibitory factor in gastritis induced by helicobacter Pylori | ||||||
| dc.type | Article |
Author Affiliations
- Guangdong Provincial People's Hospital
- The University of Hong Kong
- Sun Yat-Sen University
- Yale University School of Medicine