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Article: Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury

TitleIdentification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury
Authors
KeywordsCELLIMMUNO
HUMDISEASE
Issue Date2008
PublisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/cell
Citation
Cell, 2008, v. 133 n. 2, p. 235-249 How to Cite?
AbstractMultiple lung pathogens such as chemical agents, H5N1 avian flu, or SARS cause high lethality due to acute respiratory distress syndrome. Here we report that Toll-like receptor 4 (TLR4) mutant mice display natural resistance to acid-induced acute lung injury (ALI). We show that TLR4-TRIF-TRAF6 signaling is a key disease pathway that controls the severity of ALI. The oxidized phospholipid (OxPL) OxPAPC was identified to induce lung injury and cytokine production by lung macrophages via TLR4-TRIF. We observed OxPL production in the lungs of humans and animals infected with SARS, Anthrax, or H5N1. Pulmonary challenge with an inactivated H5N1 avian influenza virus rapidly induces ALI and OxPL formation in mice. Loss of TLR4 or TRIF expression protects mice from H5N1-induced ALI. Moreover, deletion of ncf1, which controls ROS production, improves the severity of H5N1-mediated ALI. Our data identify oxidative stress and innate immunity as key lung injury pathways that control the severity of ALI. © 2008 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/79106
ISSN
2015 Impact Factor: 28.71
2015 SCImago Journal Rankings: 28.188
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorImai, Yen_HK
dc.contributor.authorKuba, Ken_HK
dc.contributor.authorNeely, GGen_HK
dc.contributor.authorYaghubianMalhami, Ren_HK
dc.contributor.authorPerkmann, Ten_HK
dc.contributor.authorvan Loo, Gen_HK
dc.contributor.authorErmolaeva, Men_HK
dc.contributor.authorVeldhuizen, Ren_HK
dc.contributor.authorLeung, YHCen_HK
dc.contributor.authorWang, Hen_HK
dc.contributor.authorLiu, Hen_HK
dc.contributor.authorSun, Yen_HK
dc.contributor.authorPasparakis, Men_HK
dc.contributor.authorKopf, Men_HK
dc.contributor.authorMech, Cen_HK
dc.contributor.authorBavari, Sen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorSlutsky, ASen_HK
dc.contributor.authorAkira, Sen_HK
dc.contributor.authorHultqvist, Men_HK
dc.contributor.authorHolmdahl, Ren_HK
dc.contributor.authorNicholls, Jen_HK
dc.contributor.authorJiang, Cen_HK
dc.contributor.authorBinder, CJen_HK
dc.contributor.authorPenninger, JMen_HK
dc.date.accessioned2010-09-06T07:50:39Z-
dc.date.available2010-09-06T07:50:39Z-
dc.date.issued2008en_HK
dc.identifier.citationCell, 2008, v. 133 n. 2, p. 235-249en_HK
dc.identifier.issn0092-8674en_HK
dc.identifier.urihttp://hdl.handle.net/10722/79106-
dc.description.abstractMultiple lung pathogens such as chemical agents, H5N1 avian flu, or SARS cause high lethality due to acute respiratory distress syndrome. Here we report that Toll-like receptor 4 (TLR4) mutant mice display natural resistance to acid-induced acute lung injury (ALI). We show that TLR4-TRIF-TRAF6 signaling is a key disease pathway that controls the severity of ALI. The oxidized phospholipid (OxPL) OxPAPC was identified to induce lung injury and cytokine production by lung macrophages via TLR4-TRIF. We observed OxPL production in the lungs of humans and animals infected with SARS, Anthrax, or H5N1. Pulmonary challenge with an inactivated H5N1 avian influenza virus rapidly induces ALI and OxPL formation in mice. Loss of TLR4 or TRIF expression protects mice from H5N1-induced ALI. Moreover, deletion of ncf1, which controls ROS production, improves the severity of H5N1-mediated ALI. Our data identify oxidative stress and innate immunity as key lung injury pathways that control the severity of ALI. © 2008 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/cellen_HK
dc.relation.ispartofCellen_HK
dc.subjectCELLIMMUNOen_HK
dc.subjectHUMDISEASEen_HK
dc.subject.meshAdaptor Proteins, Vesicular Transport - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInfluenza, Human - metabolismen_HK
dc.subject.meshInterleukin-6 - metabolismen_HK
dc.subject.meshLungen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshNADPH Oxidase - metabolismen_HK
dc.subject.meshNF-kappa B - metabolismen_HK
dc.subject.meshOrthomyxoviridae Infections - metabolismen_HK
dc.subject.meshOxidative Stressen_HK
dc.subject.meshPhospholipids - metabolismen_HK
dc.subject.meshRespiratory Distress Syndrome, Adult - metabolismen_HK
dc.subject.meshSevere Acute Respiratory Syndrome - metabolismen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshToll-Like Receptor 4 - metabolismen_HK
dc.titleIdentification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0092-8674&volume=133&issue=2&spage=235&epage=249&date=2008&atitle=Identification+of+oxidative+stress+and+Toll-like+receptor+4+signaling+as+a+key+pathway+of+acute+lung+injury.en_HK
dc.identifier.emailLeung, YHC: cyhleung@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.emailNicholls, J: jmnichol@hkucc.hku.hken_HK
dc.identifier.authorityLeung, YHC=rp00307en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.identifier.authorityNicholls, J=rp00364en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cell.2008.02.043en_HK
dc.identifier.pmid18423196-
dc.identifier.scopuseid_2-s2.0-41949087380en_HK
dc.identifier.hkuros146234en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-41949087380&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume133en_HK
dc.identifier.issue2en_HK
dc.identifier.spage235en_HK
dc.identifier.epage249en_HK
dc.identifier.isiWOS:000255052000014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.f10005405956-
dc.identifier.scopusauthoridImai, Y=7403992303en_HK
dc.identifier.scopusauthoridKuba, K=8683968300en_HK
dc.identifier.scopusauthoridNeely, GG=22941514000en_HK
dc.identifier.scopusauthoridYaghubianMalhami, R=35314435900en_HK
dc.identifier.scopusauthoridPerkmann, T=8904629500en_HK
dc.identifier.scopusauthoridvan Loo, G=6603335624en_HK
dc.identifier.scopusauthoridErmolaeva, M=24467964600en_HK
dc.identifier.scopusauthoridVeldhuizen, R=7006488684en_HK
dc.identifier.scopusauthoridLeung, YHC=26531438300en_HK
dc.identifier.scopusauthoridWang, H=35767104400en_HK
dc.identifier.scopusauthoridLiu, H=35314338500en_HK
dc.identifier.scopusauthoridSun, Y=7406431357en_HK
dc.identifier.scopusauthoridPasparakis, M=6701908718en_HK
dc.identifier.scopusauthoridKopf, M=7004312740en_HK
dc.identifier.scopusauthoridMech, C=35314332200en_HK
dc.identifier.scopusauthoridBavari, S=7003364755en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridSlutsky, AS=35227997700en_HK
dc.identifier.scopusauthoridAkira, S=35396685700en_HK
dc.identifier.scopusauthoridHultqvist, M=8662948600en_HK
dc.identifier.scopusauthoridHolmdahl, R=7103259084en_HK
dc.identifier.scopusauthoridNicholls, J=7201463077en_HK
dc.identifier.scopusauthoridJiang, C=35076200700en_HK
dc.identifier.scopusauthoridBinder, CJ=7102159532en_HK
dc.identifier.scopusauthoridPenninger, JM=35419243000en_HK

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