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Article: Macrophage migration inhibitory factor is an important mediator in the pathoenesis of gastric inflammation in rats

TitleMacrophage migration inhibitory factor is an important mediator in the pathoenesis of gastric inflammation in rats
Authors
Issue Date2001
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
Gastroenterology, 2001, v. 121 n. 3, p. 619-630 How to Cite?
AbstractBACKGROUND and AIMS: Macrophage migration inhibitory factor (MIF) has been shown to play a pivotal role in inflammatory and immune-mediated diseases. This study investigates the role of MIF in gastric inflammation. METHODS: Expression of MIF was examined in a rat gastric ulcer model induced by acetic acid, and the functional role of MIF in acute gastric ulcer was investigated by administration of a neutralizing anti-MIF antibody. RESULTS: MIF messenger RNA and protein were markedly up-regulated in acute gastric ulcer, which correlated with the accumulation of macrophages (P < 0.001) and neutrophils (P < 0.05) at the site of inflammation. Macrophages, like neutrophils, were the major inflammatory cells infiltrating the ulcer base and they strongly expressed inducible nitric oxide synthase. However, macrophages, not neutrophils, were a rich source of MIF production in acute gastric ulcer. In vivo and in vitro blockade of MIF with the neutralizing anti-MIF antibody significantly inhibited the marked up-regulation of MIF, tumor necrosis factor alpha, inducible nitric oxide synthase, and intercellular adhesion molecule-1. This was associated with the marked inhibition of macrophage (70% reduced) and neutrophil (60% reduced) accumulation and activation, thus reducing ulcer sizes and attenuating ulceration. CONCLUSIONS: This study has shown that MIF was markedly up-regulated during acute gastric ulcer. Inhibition of acute gastric ulcer by blockade of MIF indicates that MIF is a key inflammatory mediator and plays a pathogenic role in gastric inflammation.
Persistent Identifierhttp://hdl.handle.net/10722/78160
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHuang, XRen_HK
dc.contributor.authorHui, CWCen_HK
dc.contributor.authorChen, YXen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorMetz, Cen_HK
dc.contributor.authorCho, CHen_HK
dc.contributor.authorHui, WMen_HK
dc.contributor.authorBucala, Ren_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorChun, Ben_HK
dc.contributor.authorWong, Yen_HK
dc.date.accessioned2010-09-06T07:39:50Z-
dc.date.available2010-09-06T07:39:50Z-
dc.date.issued2001en_HK
dc.identifier.citationGastroenterology, 2001, v. 121 n. 3, p. 619-630en_HK
dc.identifier.issn0016-5085en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78160-
dc.description.abstractBACKGROUND and AIMS: Macrophage migration inhibitory factor (MIF) has been shown to play a pivotal role in inflammatory and immune-mediated diseases. This study investigates the role of MIF in gastric inflammation. METHODS: Expression of MIF was examined in a rat gastric ulcer model induced by acetic acid, and the functional role of MIF in acute gastric ulcer was investigated by administration of a neutralizing anti-MIF antibody. RESULTS: MIF messenger RNA and protein were markedly up-regulated in acute gastric ulcer, which correlated with the accumulation of macrophages (P < 0.001) and neutrophils (P < 0.05) at the site of inflammation. Macrophages, like neutrophils, were the major inflammatory cells infiltrating the ulcer base and they strongly expressed inducible nitric oxide synthase. However, macrophages, not neutrophils, were a rich source of MIF production in acute gastric ulcer. In vivo and in vitro blockade of MIF with the neutralizing anti-MIF antibody significantly inhibited the marked up-regulation of MIF, tumor necrosis factor alpha, inducible nitric oxide synthase, and intercellular adhesion molecule-1. This was associated with the marked inhibition of macrophage (70% reduced) and neutrophil (60% reduced) accumulation and activation, thus reducing ulcer sizes and attenuating ulceration. CONCLUSIONS: This study has shown that MIF was markedly up-regulated during acute gastric ulcer. Inhibition of acute gastric ulcer by blockade of MIF indicates that MIF is a key inflammatory mediator and plays a pathogenic role in gastric inflammation.-
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastroen_HK
dc.relation.ispartofGastroenterologyen_HK
dc.subject.meshAntibodies, Monoclonal - pharmacology-
dc.subject.meshGastritis - etiology - immunology - metabolism-
dc.subject.meshMacrophage Migration-Inhibitory Factors - genetics - immunology - metabolism-
dc.subject.meshStomach Ulcer - etiology - immunology - metabolism-
dc.subject.meshTumor Necrosis Factor-alpha - genetics-
dc.titleMacrophage migration inhibitory factor is an important mediator in the pathoenesis of gastric inflammation in ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0016-5085&volume=121&issue=3&spage=619&epage=630&date=2001&atitle=Macrophage+migration+inhibitory+factor+is+an+important+mediator+in+the+pathoenesis+of+gastric+inflammation+in+ratsen_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.emailFung, PCW: hrspfcw@hku.hken_HK
dc.identifier.emailCho, CH: chcho@hkusua.hku.hken_HK
dc.identifier.emailHui, WM: hrmehwm@hkucc.hku.hken_HK
dc.identifier.emailLam, SK: hrmelsk@hkucc.hku.hken_HK
dc.identifier.emailLan, HY: hylan@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.identifier.doi10.1053/gast.2001.27205-
dc.identifier.pmid11522746-
dc.identifier.hkuros72117en_HK
dc.identifier.volume121-
dc.identifier.issue3-
dc.identifier.spage619-
dc.identifier.epage630-
dc.identifier.isiWOS:000170750800016-
dc.publisher.placeUnited States-

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