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Article: Alveolar macrophages are indispensable for controlling influenza viruses in lungs of pigs

TitleAlveolar macrophages are indispensable for controlling influenza viruses in lungs of pigs
Authors
Issue Date2008
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2008, v. 82 n. 9, p. 4265-4274 How to Cite?
AbstractAlveolar macrophages constitutively reside in the respiratory tracts of pigs and humans. An in vivo role of alveolar macrophages in defending against influenza viruses in mice infected with a reasserted influenza virus, 1918 HA/NA:Tx/91, was reported, but there has been no report on an in vivo role of alveolar macrophages in a natural host such as a pig using currently circulating human influenza virus. Here we show that in vivo depletion of alveolar macrophages in pigs by dichloromethylene diphosphonate (MDPCL2) treatment results in 40% mortality when pigs are infected with currently circulating human H1N1 influenza viruses, while none of the infected control pigs died. All infected pigs depleted of alveolar macrophages suffered from more severe respiratory signs than infected control pigs. Induction of tumor necrosis factor alpha in the infected pigs depleted of alveolar macrophages was significantly lower than that in the lungs of infected control pigs, and the induction of interleukin-10, an immunosuppressive cytokine, significantly increased in the lungs of infected pigs depleted of alveolar macrophages compared to infected control pigs. When we measured antibody titers and CD8+ T lymphocytes expressing gamma interferon (IFN-γ), lower antibody titers and a lower percentage of CD8+ T lymphocytes expressing IFN-γ were detectable in MDPCL2-treated infected pigs than in phosphate-buffered saline- and liposome-treated and infected pigs. Taken together, our findings suggest that alveolar macrophages are essential for controlling H1N1 influenza viruses in pigs. Copyright © 2008, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179809
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHeui, MKen_US
dc.contributor.authorLee, YWen_US
dc.contributor.authorLee, KJen_US
dc.contributor.authorHyun, SKen_US
dc.contributor.authorSung, WCen_US
dc.contributor.authorVan Rooijen, Nen_US
dc.contributor.authorGuan, Yen_US
dc.contributor.authorSang, HSen_US
dc.date.accessioned2012-12-19T10:05:01Z-
dc.date.available2012-12-19T10:05:01Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Virology, 2008, v. 82 n. 9, p. 4265-4274en_US
dc.identifier.issn0022-538Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/179809-
dc.description.abstractAlveolar macrophages constitutively reside in the respiratory tracts of pigs and humans. An in vivo role of alveolar macrophages in defending against influenza viruses in mice infected with a reasserted influenza virus, 1918 HA/NA:Tx/91, was reported, but there has been no report on an in vivo role of alveolar macrophages in a natural host such as a pig using currently circulating human influenza virus. Here we show that in vivo depletion of alveolar macrophages in pigs by dichloromethylene diphosphonate (MDPCL2) treatment results in 40% mortality when pigs are infected with currently circulating human H1N1 influenza viruses, while none of the infected control pigs died. All infected pigs depleted of alveolar macrophages suffered from more severe respiratory signs than infected control pigs. Induction of tumor necrosis factor alpha in the infected pigs depleted of alveolar macrophages was significantly lower than that in the lungs of infected control pigs, and the induction of interleukin-10, an immunosuppressive cytokine, significantly increased in the lungs of infected pigs depleted of alveolar macrophages compared to infected control pigs. When we measured antibody titers and CD8+ T lymphocytes expressing gamma interferon (IFN-γ), lower antibody titers and a lower percentage of CD8+ T lymphocytes expressing IFN-γ were detectable in MDPCL2-treated infected pigs than in phosphate-buffered saline- and liposome-treated and infected pigs. Taken together, our findings suggest that alveolar macrophages are essential for controlling H1N1 influenza viruses in pigs. Copyright © 2008, American Society for Microbiology. All Rights Reserved.en_US
dc.languageengen_US
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_US
dc.relation.ispartofJournal of Virologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCd8-Positive T-Lymphocytes - Immunologyen_US
dc.subject.meshClodronic Acid - Pharmacologyen_US
dc.subject.meshGene Expression Regulation - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInfluenza A Virus, H1n1 Subtype - Immunologyen_US
dc.subject.meshInterleukin-10 - Geneticsen_US
dc.subject.meshLung Diseases - Immunology - Virologyen_US
dc.subject.meshMacrophages, Alveolar - Drug Effects - Immunologyen_US
dc.subject.meshOrthomyxoviridae - Immunologyen_US
dc.subject.meshOrthomyxoviridae Infections - Immunologyen_US
dc.subject.meshSwineen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Geneticsen_US
dc.titleAlveolar macrophages are indispensable for controlling influenza viruses in lungs of pigsen_US
dc.typeArticleen_US
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_US
dc.identifier.authorityGuan, Y=rp00397en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1128/JVI.02602-07en_US
dc.identifier.pmid18287245-
dc.identifier.scopuseid_2-s2.0-42449095509en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-42449095509&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume82en_US
dc.identifier.issue9en_US
dc.identifier.spage4265en_US
dc.identifier.epage4274en_US
dc.identifier.isiWOS:000255084600008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHeui, MK=24075766700en_US
dc.identifier.scopusauthoridLee, YW=8983566800en_US
dc.identifier.scopusauthoridLee, KJ=35311016000en_US
dc.identifier.scopusauthoridHyun, SK=37042958800en_US
dc.identifier.scopusauthoridSung, WC=24077422600en_US
dc.identifier.scopusauthoridVan Rooijen, N=35428581800en_US
dc.identifier.scopusauthoridGuan, Y=7202924055en_US
dc.identifier.scopusauthoridSang, HS=7202469843en_US
dc.identifier.citeulike2667731-

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