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Article: Helicobacter pylori infection is associated with increased expression of macrophage migratory inhibitory factor - by epithelial cells, T cells, and macrophages - in gastric mucosa

TitleHelicobacter pylori infection is associated with increased expression of macrophage migratory inhibitory factor - by epithelial cells, T cells, and macrophages - in gastric mucosa
Authors
Issue Date2004
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2004, v. 190 n. 2, p. 293-302 How to Cite?
AbstractThe macrophage migratory inhibitory factor (MIF) plays a pivotal role in inflammatory and immune diseases; however, its role in gastrointestinal diseases has not been clarified. This study intended to determine the expression of MIF, by gastric epithelial cells, T cells, and macrophages, in Helicobacter pylori-induced gastritis. Sixty-four patients (30 males, 34 females; mean age, 47 years) referred for upper endoscopy were recruited. Biopsy specimens from the gastric antrum and corpus were obtained for (1) detection of H. pylori and histological examination, (2) single and double immunostaining to test for expression of MIF protein in epithelial cells, T cells, and macrophages, and (2) in situ hybridization for expression of MIF mRNA within the lamina propria. In mucosal specimens from each of the 2 sites, both the percentage of MIF + epithelial cells and the numbers of MIF mRNA+ inflammatory cells, MIF+ T cells, and MIF+ macrophages were significantly higher in H. pylori-positive patients than in H. pylori-negative patients. Overall, the percentage of MIF+ epithelial cells and the numbers of MIF mRNA+ cells, MIF+ T cells, and MIF+ macrophages were higher in the antrum than in the corpus. The percentage of MIF+ epithelial cells and the numbers of MIF mRNA+ cells, MIF+ T cells, and MIF+ macrophages increased in chronic gastritis, but, in the absence of H. pylori infection, this increase disappeared for all except MIF+ T cells. Therefore, H. pylori infection is associated with increased expression of the MIF protein and MIF mRNA in gastric epithelial and inflammatory cells; along with other cytokines, MIF may play a significant role in gastric inflammation related to H. pylori infection.
Persistent Identifierhttp://hdl.handle.net/10722/43109
ISSN
2021 Impact Factor: 7.759
2020 SCImago Journal Rankings: 2.690
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorHuang, XRen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorLeung, SYen_HK
dc.contributor.authorYuen, STen_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2007-03-23T04:39:03Z-
dc.date.available2007-03-23T04:39:03Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2004, v. 190 n. 2, p. 293-302en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/43109-
dc.description.abstractThe macrophage migratory inhibitory factor (MIF) plays a pivotal role in inflammatory and immune diseases; however, its role in gastrointestinal diseases has not been clarified. This study intended to determine the expression of MIF, by gastric epithelial cells, T cells, and macrophages, in Helicobacter pylori-induced gastritis. Sixty-four patients (30 males, 34 females; mean age, 47 years) referred for upper endoscopy were recruited. Biopsy specimens from the gastric antrum and corpus were obtained for (1) detection of H. pylori and histological examination, (2) single and double immunostaining to test for expression of MIF protein in epithelial cells, T cells, and macrophages, and (2) in situ hybridization for expression of MIF mRNA within the lamina propria. In mucosal specimens from each of the 2 sites, both the percentage of MIF + epithelial cells and the numbers of MIF mRNA+ inflammatory cells, MIF+ T cells, and MIF+ macrophages were significantly higher in H. pylori-positive patients than in H. pylori-negative patients. Overall, the percentage of MIF+ epithelial cells and the numbers of MIF mRNA+ cells, MIF+ T cells, and MIF+ macrophages were higher in the antrum than in the corpus. The percentage of MIF+ epithelial cells and the numbers of MIF mRNA+ cells, MIF+ T cells, and MIF+ macrophages increased in chronic gastritis, but, in the absence of H. pylori infection, this increase disappeared for all except MIF+ T cells. Therefore, H. pylori infection is associated with increased expression of the MIF protein and MIF mRNA in gastric epithelial and inflammatory cells; along with other cytokines, MIF may play a significant role in gastric inflammation related to H. pylori infection.en_HK
dc.format.extent646919 bytes-
dc.format.extent284160 bytes-
dc.format.extent270804 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
dc.format.mimetypeapplication/pdf-
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org en_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.rightsJournal of Infectious Diseases. Copyright © University of Chicago Press.en_HK
dc.subject.meshGastric mucosa - immunology - microbiology - pathologyen_HK
dc.subject.meshHelicobacter infections - immunology - microbiologyen_HK
dc.subject.meshHelicobacter pylorien_HK
dc.subject.meshMacrophage migration-inhibitory factors - genetics - metabolismen_HK
dc.subject.meshMacrophages - immunologyen_HK
dc.titleHelicobacter pylori infection is associated with increased expression of macrophage migratory inhibitory factor - by epithelial cells, T cells, and macrophages - in gastric mucosaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1899&volume=190&issue=2&spage=293&epage=302&date=2004&atitle=Helicobacter+pylori+infection+is+associated+with+increased+expression+of+macrophage+migratory+inhibitory+factor--by+epithelial+cells,+T+cells,+and+macrophages--in+gastric+mucosaen_HK
dc.identifier.emailLeung, SY:suetyi@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1086/421915en_HK
dc.identifier.pmid15216464-
dc.identifier.scopuseid_2-s2.0-3242656101en_HK
dc.identifier.hkuros89844-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3242656101&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume190en_HK
dc.identifier.issue2en_HK
dc.identifier.spage293en_HK
dc.identifier.epage302en_HK
dc.identifier.isiWOS:000222254800012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK
dc.identifier.scopusauthoridHuang, XR=7410248090en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridLeung, SY=7202044886en_HK
dc.identifier.scopusauthoridYuen, ST=36921609700en_HK
dc.identifier.scopusauthoridLan, HY=7102710832en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.issnl0022-1899-

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