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Article: Mannose-binding lectin contributes to deleterious inflammatory response in pandemic H1N1 and avian H9N2 infection

TitleMannose-binding lectin contributes to deleterious inflammatory response in pandemic H1N1 and avian H9N2 infection
Authors
Issue Date2012
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2012, v. 205 n. 1, p. 44-53 How to Cite?
AbstractBackground. Mannose-binding lectin (MBL) is a pattern-recognition molecule, which functions as a first line of host defense. Pandemic H1N1 (pdmH1N1) influenza A virus caused massive infection in 2009 and currently circulates worldwide. Avian influenza A H9N2 (H9N2/G1) virus has infected humans and has the potential to be the next pandemic virus. Antiviral function and immunomodulatory role of MBL in pdmH1N1 and H9N2/G1 virus infection have not been investigated. Methods. In this study, MBL wild-type (WT) and MBL knockout (KO) murine models were used to examine the role of MBL in pdmH1N1 and H9N2/G1 virus infection. Results. Our study demonstrated that in vitro, MBL binds to pdmH1N1 and H9N2/G1 viruses, likely via the carbohydrate recognition domain of MBL. Wild-type mice developed more severe disease, as evidenced by a greater weight loss than MBL KO mice during influenza virus infection. Furthermore, MBL WT mice had enhanced production of proinflammatory cytokines and chemokines compared with MBL KO mice, suggesting that MBL could upregulate inflammatory responses that may potentially worsen pdmH1N1 and H9N2/G1 virus infections. Conclusions. Our study provided the first in vivo evidence that MBL may be a risk factor during pdmH1N1 and H9N2/G1 infection by upregulating proinflammatory response. © 2011 The Author.
Persistent Identifierhttp://hdl.handle.net/10722/146346
ISSN
2015 Impact Factor: 6.344
2015 SCImago Journal Rankings: 4.000
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
National Institutes of HealthU01AI074503
University Grants Committee of the Hong Kong Special Administrative Region, ChinaAoE/M-12/06
Hong Kong SAR governmentLab-11
Chung Ko Lee and Cheung Yuen Kan Education and Research Fund in Paediatric Immunology
Funding Information:

This work was supported in part by the National Institutes of Health (U01AI074503); the Area of Excellence program on influenza supported by the University Grants Committee of the Hong Kong Special Administrative Region, China (AoE/M-12/06); the Research Fund for the Control of Infectious Diseases, Hong Kong SAR government (Lab-11); and the Chung Ko Lee and Cheung Yuen Kan Education and Research Fund in Paediatric Immunology.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorLing, MTen_HK
dc.contributor.authorTu, Wen_HK
dc.contributor.authorHan, Yen_HK
dc.contributor.authorMao, Hen_HK
dc.contributor.authorChong, WPen_HK
dc.contributor.authorGuan, Jen_HK
dc.contributor.authorLiu, Men_HK
dc.contributor.authorLam, KTen_HK
dc.contributor.authorLaw, HKWen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorTakahashi, Ken_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2012-04-20T02:05:12Z-
dc.date.available2012-04-20T02:05:12Z-
dc.date.issued2012en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2012, v. 205 n. 1, p. 44-53en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146346-
dc.description.abstractBackground. Mannose-binding lectin (MBL) is a pattern-recognition molecule, which functions as a first line of host defense. Pandemic H1N1 (pdmH1N1) influenza A virus caused massive infection in 2009 and currently circulates worldwide. Avian influenza A H9N2 (H9N2/G1) virus has infected humans and has the potential to be the next pandemic virus. Antiviral function and immunomodulatory role of MBL in pdmH1N1 and H9N2/G1 virus infection have not been investigated. Methods. In this study, MBL wild-type (WT) and MBL knockout (KO) murine models were used to examine the role of MBL in pdmH1N1 and H9N2/G1 virus infection. Results. Our study demonstrated that in vitro, MBL binds to pdmH1N1 and H9N2/G1 viruses, likely via the carbohydrate recognition domain of MBL. Wild-type mice developed more severe disease, as evidenced by a greater weight loss than MBL KO mice during influenza virus infection. Furthermore, MBL WT mice had enhanced production of proinflammatory cytokines and chemokines compared with MBL KO mice, suggesting that MBL could upregulate inflammatory responses that may potentially worsen pdmH1N1 and H9N2/G1 virus infections. Conclusions. Our study provided the first in vivo evidence that MBL may be a risk factor during pdmH1N1 and H9N2/G1 infection by upregulating proinflammatory response. © 2011 The Author.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.orgen_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.subject.meshInflammation - immunology - metabolism-
dc.subject.meshInfluenza A Virus, H1N1 Subtype - immunology - metabolism-
dc.subject.meshInfluenza A Virus, H9N2 Subtype - immunology - metabolism-
dc.subject.meshMannose-Binding Lectin - immunology - metabolism-
dc.subject.meshOrthomyxoviridae Infections - immunology - metabolism - pathology - virology-
dc.titleMannose-binding lectin contributes to deleterious inflammatory response in pandemic H1N1 and avian H9N2 infectionen_HK
dc.typeArticleen_HK
dc.identifier.emailTu, W: wwtu@hku.hken_HK
dc.identifier.emailMao, H: hwmau@hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.authorityTu, W=rp00416en_HK
dc.identifier.authorityMao, H=rp01595en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/infdis/jir691en_HK
dc.identifier.pmid22080095-
dc.identifier.pmcidPMC3242741-
dc.identifier.scopuseid_2-s2.0-84555189246en_HK
dc.identifier.hkuros200718-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84555189246&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume205en_HK
dc.identifier.issue1en_HK
dc.identifier.spage44en_HK
dc.identifier.epage53en_HK
dc.identifier.eissn1537-6613-
dc.identifier.isiWOS:000298386200009-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectControl of Pandemic and Inter-pandemic Influenza-
dc.identifier.scopusauthoridLing, MT=44761279100en_HK
dc.identifier.scopusauthoridTu, W=7006479236en_HK
dc.identifier.scopusauthoridHan, Y=54795161300en_HK
dc.identifier.scopusauthoridMao, H=25632489000en_HK
dc.identifier.scopusauthoridChong, WP=8634104400en_HK
dc.identifier.scopusauthoridGuan, J=36243371100en_HK
dc.identifier.scopusauthoridLiu, M=55210686600en_HK
dc.identifier.scopusauthoridLam, KT=25630903400en_HK
dc.identifier.scopusauthoridLaw, HKW=7101939394en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridTakahashi, K=8586134200en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK

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