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Article: Macrophage migration inhibitory factor stimulated by Helicobacter pylori increases proliferation of gastric epithelial cells

TitleMacrophage migration inhibitory factor stimulated by Helicobacter pylori increases proliferation of gastric epithelial cells
Authors
KeywordsH pylori
MIF
PAI
Issue Date2005
PublisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htm
Citation
World Journal Of Gastroenterology, 2005, v. 11 n. 13, p. 1946-1950 How to Cite?
AbstractAim: Helicobacter pylori (H pylori) is associated with increased gastric inflammatory and epithelial expression of macrophage migration inhibitory factor (MIF) and gastric epithelial cell proliferation. This study aimed at determining whether H pylori directly stimulates release of MIF in monocytes, whether the cag pathogenicity island (PAI) is involved for this function, and whether MIF stimulated by H pylori increases gastric epithelial cell proliferation in vitro. Methods: A cytotoxic wild-type H pylori strain (TN2), its three isogenic mutants (TN2Δcag, TN2ΔcagA and TN2ΔcagE) were co-cultured with cells of a human monocyte cell line, THP-1, for 24 h at different organism/cell ratios. MIF in the supernatants was measured by an ELISA. Cells of a human gastric cancer cell line, MKN45, were then co-cultured with the supernatants, with and without monoclonal anti-MIF antibody for 24 h. The cells were further incubated for 12 h after addition of 3H-thymidine, and the levels of incorporation of 3H-thymidine were measured with a liquid scintillation counter. Results: The wild-type strain and the isogenic mutants, TN2ΔcagA and TN2ΔcagE, increased MIF release at organism/cell ratios of 200 /1 and 400/1, but not at the ratios of 50/1 and 100/1. However, the mutant TN2Δcag did not increase the release of MIF at any of the four ratios. 3H-thymidine readings for MKN-45 cells were significantly increased with supernatants derived from the wild-type strain and the mutants TN2ΔcagA and TN2ΔcagE, but not from the mutant TN2Δcag. Moreover, in the presence of monoclonal anti-MIF antibody, the stimulatory effects of the wild-type strain on cell proliferation disappeared. Conclusion: H pylori stimulates MIF release in monocytes, likely through its cag PAI, but not related to cagA or cagE. H pylori-stimulated monocyte culture supernatant increases gastric cell proliferation, which is blocked by anti-MIF antibody, suggesting that MIF plays an important role in H pylori-induced gastric epithelial cell proliferation. © 2005 The WJG Press and Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/76380
ISSN
2015 Impact Factor: 2.787
2015 SCImago Journal Rankings: 1.076
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorChan, AOOen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorOgura, Ken_HK
dc.contributor.authorBerg, DEen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T07:20:36Z-
dc.date.available2010-09-06T07:20:36Z-
dc.date.issued2005en_HK
dc.identifier.citationWorld Journal Of Gastroenterology, 2005, v. 11 n. 13, p. 1946-1950en_HK
dc.identifier.issn1007-9327en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76380-
dc.description.abstractAim: Helicobacter pylori (H pylori) is associated with increased gastric inflammatory and epithelial expression of macrophage migration inhibitory factor (MIF) and gastric epithelial cell proliferation. This study aimed at determining whether H pylori directly stimulates release of MIF in monocytes, whether the cag pathogenicity island (PAI) is involved for this function, and whether MIF stimulated by H pylori increases gastric epithelial cell proliferation in vitro. Methods: A cytotoxic wild-type H pylori strain (TN2), its three isogenic mutants (TN2Δcag, TN2ΔcagA and TN2ΔcagE) were co-cultured with cells of a human monocyte cell line, THP-1, for 24 h at different organism/cell ratios. MIF in the supernatants was measured by an ELISA. Cells of a human gastric cancer cell line, MKN45, were then co-cultured with the supernatants, with and without monoclonal anti-MIF antibody for 24 h. The cells were further incubated for 12 h after addition of 3H-thymidine, and the levels of incorporation of 3H-thymidine were measured with a liquid scintillation counter. Results: The wild-type strain and the isogenic mutants, TN2ΔcagA and TN2ΔcagE, increased MIF release at organism/cell ratios of 200 /1 and 400/1, but not at the ratios of 50/1 and 100/1. However, the mutant TN2Δcag did not increase the release of MIF at any of the four ratios. 3H-thymidine readings for MKN-45 cells were significantly increased with supernatants derived from the wild-type strain and the mutants TN2ΔcagA and TN2ΔcagE, but not from the mutant TN2Δcag. Moreover, in the presence of monoclonal anti-MIF antibody, the stimulatory effects of the wild-type strain on cell proliferation disappeared. Conclusion: H pylori stimulates MIF release in monocytes, likely through its cag PAI, but not related to cagA or cagE. H pylori-stimulated monocyte culture supernatant increases gastric cell proliferation, which is blocked by anti-MIF antibody, suggesting that MIF plays an important role in H pylori-induced gastric epithelial cell proliferation. © 2005 The WJG Press and Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htmen_HK
dc.relation.ispartofWorld Journal of Gastroenterologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectH pylorien_HK
dc.subjectMIFen_HK
dc.subjectPAIen_HK
dc.subject.meshAntibodies, Monoclonal - pharmacologyen_HK
dc.subject.meshAntigens, Bacterial - geneticsen_HK
dc.subject.meshBacterial Proteins - geneticsen_HK
dc.subject.meshCell Division - physiologyen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshEpithelial Cells - metabolism - microbiology - pathologyen_HK
dc.subject.meshHelicobacter Infections - pathologyen_HK
dc.subject.meshHelicobacter pylori - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMacrophage Migration-Inhibitory Factors - immunology - metabolismen_HK
dc.subject.meshMonocytes - cytology - microbiologyen_HK
dc.subject.meshMutationen_HK
dc.subject.meshStomach - microbiology - pathologyen_HK
dc.titleMacrophage migration inhibitory factor stimulated by Helicobacter pylori increases proliferation of gastric epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1007-9327&volume=11&issue=13&spage=1946&epage=1950&date=2005&atitle=Macrophage+Migration+Inhibitory+Factor+Stimulated+by+Helicobacter+pylori+Increases+Proliferation+of+Gastric+Epithelial+Cellsen_HK
dc.identifier.emailLin, MCM:mcllin@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3748/wjg.v11.i13.1946-
dc.identifier.pmid15800984-
dc.identifier.pmcidPMC4305715-
dc.identifier.scopuseid_2-s2.0-17144383252en_HK
dc.identifier.hkuros97727en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-17144383252&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue13en_HK
dc.identifier.spage1946en_HK
dc.identifier.epage1950en_HK
dc.identifier.isiWOS:000208102500009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK
dc.identifier.scopusauthoridChan, AOO=7403167965en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridOgura, K=7401552682en_HK
dc.identifier.scopusauthoridBerg, DE=7202401139en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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