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Article: Role for macrophage migration inhibitory factor in acute respiratory distress syndrome

TitleRole for macrophage migration inhibitory factor in acute respiratory distress syndrome
Authors
KeywordsAcute respiratory distress syndrome
Anti-MIF
Aquaporin 1
Glucocorticoid
Macrophage migration inhibitory factor
Tumour necrosis factor-α
Issue Date2003
PublisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130
Citation
Journal Of Pathology, 2003, v. 199 n. 4, p. 496-508 How to Cite?
AbstractThe critical role of macrophage migration inhibitory factor (MIF) in mediating inflammatory lung injury in acute respiratory distress syndrome (ARDS) has been raised recently. The present study has identified enhanced MIF protein expression in alveolar capillary endothelium and infiltrating macrophages in lung tissues from ARDS patients. The possibility that MIF up-regulates its synthesis in an autocrine fashion in ARDS was tested using cultured endothelial cells stimulated with MIF and a murine model of lipopolysaccharide (LPS)-induced acute lung injury. MIF induced significant MIF and tumour necrosis factor (TNF)-α synthesis in cultured endothelial cells and the effect was blocked by neutralizing anti-MIF antibody. A similar blocking effect was observed when MIF-stimulated endothelial cells were pretreated with neutralizing anti-TNF-α antibody or glucocorticoid, supporting the notion that MIF induced TNF-α production via an amplifying pro-inflammatory loop. Treatment with anti-MIF or glucocorticoid effectively attenuated pulmonary pathology and the synthesis of MIF or TNF-α in mice with LPS-induced acute lung injury. Mildly augmented expression of aquaporin 1 (AQP1) was also detected in alveolar capillary endothelium in ARDS. In vitro studies revealed that both MIF and TNF-α induced a small increase of AQP1 synthesis in cultured endothelial cells. These findings suggest that MIF plays a crucial pathological role leading to alveolar inflammation in ARDS. Anti-MIF and early glucocorticoid therapy may represent a novel therapeutic approach for reducing alveolar inflammation in ARDS. Copyright © 2003 John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/78614
ISSN
2015 Impact Factor: 7.381
2015 SCImago Journal Rankings: 4.176
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorMetz, CNen_HK
dc.contributor.authorLai, FMen_HK
dc.contributor.authorBucala, Ren_HK
dc.contributor.authorLan, HYen_HK
dc.date.accessioned2010-09-06T07:44:50Z-
dc.date.available2010-09-06T07:44:50Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Pathology, 2003, v. 199 n. 4, p. 496-508en_HK
dc.identifier.issn0022-3417en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78614-
dc.description.abstractThe critical role of macrophage migration inhibitory factor (MIF) in mediating inflammatory lung injury in acute respiratory distress syndrome (ARDS) has been raised recently. The present study has identified enhanced MIF protein expression in alveolar capillary endothelium and infiltrating macrophages in lung tissues from ARDS patients. The possibility that MIF up-regulates its synthesis in an autocrine fashion in ARDS was tested using cultured endothelial cells stimulated with MIF and a murine model of lipopolysaccharide (LPS)-induced acute lung injury. MIF induced significant MIF and tumour necrosis factor (TNF)-α synthesis in cultured endothelial cells and the effect was blocked by neutralizing anti-MIF antibody. A similar blocking effect was observed when MIF-stimulated endothelial cells were pretreated with neutralizing anti-TNF-α antibody or glucocorticoid, supporting the notion that MIF induced TNF-α production via an amplifying pro-inflammatory loop. Treatment with anti-MIF or glucocorticoid effectively attenuated pulmonary pathology and the synthesis of MIF or TNF-α in mice with LPS-induced acute lung injury. Mildly augmented expression of aquaporin 1 (AQP1) was also detected in alveolar capillary endothelium in ARDS. In vitro studies revealed that both MIF and TNF-α induced a small increase of AQP1 synthesis in cultured endothelial cells. These findings suggest that MIF plays a crucial pathological role leading to alveolar inflammation in ARDS. Anti-MIF and early glucocorticoid therapy may represent a novel therapeutic approach for reducing alveolar inflammation in ARDS. Copyright © 2003 John Wiley & Sons, Ltd.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130en_HK
dc.relation.ispartofJournal of Pathologyen_HK
dc.rightsJournal of Pathology. Copyright © John Wiley & Sons Ltd.en_HK
dc.subjectAcute respiratory distress syndromeen_HK
dc.subjectAnti-MIFen_HK
dc.subjectAquaporin 1en_HK
dc.subjectGlucocorticoiden_HK
dc.subjectMacrophage migration inhibitory factoren_HK
dc.subjectTumour necrosis factor-αen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntibodies, Monoclonal - therapeutic useen_HK
dc.subject.meshAquaporin 1en_HK
dc.subject.meshAquaporins - biosynthesisen_HK
dc.subject.meshBlood Group Antigensen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshDexamethasone - therapeutic useen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expressionen_HK
dc.subject.meshGlucocorticoids - therapeutic useen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLipopolysaccharidesen_HK
dc.subject.meshMacrophage Migration-Inhibitory Factors - biosynthesis - genetics - physiologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPulmonary Alveoli - metabolismen_HK
dc.subject.meshRNA, Messenger - geneticsen_HK
dc.subject.meshRespiratory Distress Syndrome, Adult - physiopathology - prevention & controlen_HK
dc.subject.meshTumor Necrosis Factor-alpha - biosynthesis - immunologyen_HK
dc.titleRole for macrophage migration inhibitory factor in acute respiratory distress syndromeen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3417&volume=199&spage=496&epage=508&date=2003&atitle=Role+for+Macrophage+Migration+Inhibitory+Factor+in+Acute+Respiratory+Distress+Syndromeen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/path.1291en_HK
dc.identifier.pmid12635141-
dc.identifier.scopuseid_2-s2.0-0037385935en_HK
dc.identifier.hkuros81113en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037385935&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume199en_HK
dc.identifier.issue4en_HK
dc.identifier.spage496en_HK
dc.identifier.epage508en_HK
dc.identifier.isiWOS:000181973100012-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridMetz, CN=7102876220en_HK
dc.identifier.scopusauthoridLai, FM=7202559720en_HK
dc.identifier.scopusauthoridBucala, R=7102379822en_HK
dc.identifier.scopusauthoridLan, HY=7102710832en_HK

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