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Article: Successive influenza virus infection and Streptococcus pneumoniae stimulation alter human dendritic cell function
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TitleSuccessive influenza virus infection and Streptococcus pneumoniae stimulation alter human dendritic cell function
 
AuthorsWu, Y1
Mao, H1
Ling, MT1
Chow, KH1
Ho, PL1
Tu, W1
Lau, YL1
 
Issue Date2011
 
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcinfectdis/
 
CitationBmc Infectious Diseases, 2011, v. 11 [How to Cite?]
DOI: http://dx.doi.org/10.1186/1471-2334-11-201
 
AbstractBackground: Influenza virus is a major cause of respiratory disease worldwide and Streptococcus pneumoniae infection associated with influenza often leads to severe complications. Dendritic cells are key antigen presenting cells but its role in such co-infection is unclear.Methods: In this study, human monocyte derived-dentritic cells were either concurrently or successively challenged with the combination of live influenza virus and heat killed pneumococcus to mimic the viral pneumococcal infection. Dendritic cell viability, phenotypic maturation and cytokine production were then examined.Results: The challenge of influenza virus and pneumococcus altered dendritic cell functions dependent on the time interval between the successive challenge of influenza virus and pneumococcus, as well as the doses of pneumococcus. When dendritic cells were exposed to pneumococcus at 6 hr, but not 0 hr nor 24 hr after influenza virus infection, both virus and pneumococcus treated dendritic cells had greater cell apoptosis and expressed higher CD83 and CD86 than dendritic cells infected with influenza virus alone. Dendritic cells produced pro-inflammatory cytokines: TNF-α, IL-12 and IFN-γ synergistically to the successive viral and pneumococcal challenge. Whereas prior influenza virus infection suppressed the IL-10 response independent of the timing of the subsequent pneumococcal stimulation.Conclusions: Our results demonstrated that successive challenge of dendritic cells with influenza virus and pneumococcus resulted in synergistic up-regulation of pro-inflammatory cytokines with simultaneous down-regulation of anti-inflammatory cytokine, which may explain the immuno-pathogenesis of this important co-infection. © 2011 Wu et al; licensee BioMed Central Ltd.
 
ISSN1471-2334
2013 Impact Factor: 2.561
2013 SCImago Journal Rankings: 1.420
 
DOIhttp://dx.doi.org/10.1186/1471-2334-11-201
 
PubMed Central IDPMC3146832
 
ISI Accession Number IDWOS:000293283200001
Funding AgencyGrant Number
University Grants Committee of the Hong Kong SAR, ChinaAoE/M-12/06
Research Grants Council of Hong KongHKU 777108M
HKU777407
HKU768108
Health, Welfare and Food Bureau of the Hong Kong SAR GovernmentLab-11
Edward Sai-Kim Hotung Paediatric Education and Research Fund
Funding Information:

This work was supported in part by the Area of Excellence program on Influenza supported by the University Grants Committee of the Hong Kong SAR, China (Project No AoE/M-12/06); General Research Fund, Research Grants Council of Hong Kong, (HKU 777108M, HKU777407, HKU768108); a Commission Grant from the Research Fund for the Control of Infectious Diseases (RFCID) of the Health, Welfare and Food Bureau of the Hong Kong SAR Government (2009-2014, Lab-11); Edward Sai-Kim Hotung Paediatric Education and Research Fund. Technical support of the use of flow cytometry from Faculty Core Facility.

 
ReferencesReferences in Scopus
 
GrantsControl of Pandemic and Inter-pandemic Influenza
The Role of Natural Killer Cells in the Pathogenesis of Avian Influenza Virus Infection
 
DC FieldValue
dc.contributor.authorWu, Y
 
dc.contributor.authorMao, H
 
dc.contributor.authorLing, MT
 
dc.contributor.authorChow, KH
 
dc.contributor.authorHo, PL
 
dc.contributor.authorTu, W
 
dc.contributor.authorLau, YL
 
dc.date.accessioned2011-09-23T05:51:54Z
 
dc.date.available2011-09-23T05:51:54Z
 
dc.date.issued2011
 
dc.description.abstractBackground: Influenza virus is a major cause of respiratory disease worldwide and Streptococcus pneumoniae infection associated with influenza often leads to severe complications. Dendritic cells are key antigen presenting cells but its role in such co-infection is unclear.Methods: In this study, human monocyte derived-dentritic cells were either concurrently or successively challenged with the combination of live influenza virus and heat killed pneumococcus to mimic the viral pneumococcal infection. Dendritic cell viability, phenotypic maturation and cytokine production were then examined.Results: The challenge of influenza virus and pneumococcus altered dendritic cell functions dependent on the time interval between the successive challenge of influenza virus and pneumococcus, as well as the doses of pneumococcus. When dendritic cells were exposed to pneumococcus at 6 hr, but not 0 hr nor 24 hr after influenza virus infection, both virus and pneumococcus treated dendritic cells had greater cell apoptosis and expressed higher CD83 and CD86 than dendritic cells infected with influenza virus alone. Dendritic cells produced pro-inflammatory cytokines: TNF-α, IL-12 and IFN-γ synergistically to the successive viral and pneumococcal challenge. Whereas prior influenza virus infection suppressed the IL-10 response independent of the timing of the subsequent pneumococcal stimulation.Conclusions: Our results demonstrated that successive challenge of dendritic cells with influenza virus and pneumococcus resulted in synergistic up-regulation of pro-inflammatory cytokines with simultaneous down-regulation of anti-inflammatory cytokine, which may explain the immuno-pathogenesis of this important co-infection. © 2011 Wu et al; licensee BioMed Central Ltd.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationBmc Infectious Diseases, 2011, v. 11 [How to Cite?]
DOI: http://dx.doi.org/10.1186/1471-2334-11-201
 
dc.identifier.citeulike9573224
 
dc.identifier.doihttp://dx.doi.org/10.1186/1471-2334-11-201
 
dc.identifier.hkuros192241
 
dc.identifier.hkuros192241
 
dc.identifier.hkuros200730
 
dc.identifier.isiWOS:000293283200001
Funding AgencyGrant Number
University Grants Committee of the Hong Kong SAR, ChinaAoE/M-12/06
Research Grants Council of Hong KongHKU 777108M
HKU777407
HKU768108
Health, Welfare and Food Bureau of the Hong Kong SAR GovernmentLab-11
Edward Sai-Kim Hotung Paediatric Education and Research Fund
Funding Information:

This work was supported in part by the Area of Excellence program on Influenza supported by the University Grants Committee of the Hong Kong SAR, China (Project No AoE/M-12/06); General Research Fund, Research Grants Council of Hong Kong, (HKU 777108M, HKU777407, HKU768108); a Commission Grant from the Research Fund for the Control of Infectious Diseases (RFCID) of the Health, Welfare and Food Bureau of the Hong Kong SAR Government (2009-2014, Lab-11); Edward Sai-Kim Hotung Paediatric Education and Research Fund. Technical support of the use of flow cytometry from Faculty Core Facility.

 
dc.identifier.issn1471-2334
2013 Impact Factor: 2.561
2013 SCImago Journal Rankings: 1.420
 
dc.identifier.pmcidPMC3146832
 
dc.identifier.pmid21771345
 
dc.identifier.scopuseid_2-s2.0-79960556668
 
dc.identifier.urihttp://hdl.handle.net/10722/139573
 
dc.identifier.volume11
 
dc.languageeng
 
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcinfectdis/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofBMC Infectious Diseases
 
dc.relation.projectControl of Pandemic and Inter-pandemic Influenza
 
dc.relation.projectThe Role of Natural Killer Cells in the Pathogenesis of Avian Influenza Virus Infection
 
dc.relation.referencesReferences in Scopus
 
dc.rightsBMC Infectious Diseases. Copyright © BioMed Central.
 
dc.subject.meshDendritic Cells - immunology - microbiology - virology
 
dc.subject.meshInfluenza A Virus, H1N1 Subtype - immunology
 
dc.subject.meshInfluenza, Human - immunology
 
dc.subject.meshPneumococcal Infections - immunology
 
dc.subject.meshStreptococcus pneumoniae - immunology
 
dc.titleSuccessive influenza virus infection and Streptococcus pneumoniae stimulation alter human dendritic cell function
 
dc.typeArticle
 
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<description.abstract>Background: Influenza virus is a major cause of respiratory disease worldwide and Streptococcus pneumoniae infection associated with influenza often leads to severe complications. Dendritic cells are key antigen presenting cells but its role in such co-infection is unclear.Methods: In this study, human monocyte derived-dentritic cells were either concurrently or successively challenged with the combination of live influenza virus and heat killed pneumococcus to mimic the viral pneumococcal infection. Dendritic cell viability, phenotypic maturation and cytokine production were then examined.Results: The challenge of influenza virus and pneumococcus altered dendritic cell functions dependent on the time interval between the successive challenge of influenza virus and pneumococcus, as well as the doses of pneumococcus. When dendritic cells were exposed to pneumococcus at 6 hr, but not 0 hr nor 24 hr after influenza virus infection, both virus and pneumococcus treated dendritic cells had greater cell apoptosis and expressed higher CD83 and CD86 than dendritic cells infected with influenza virus alone. Dendritic cells produced pro-inflammatory cytokines: TNF-&#945;, IL-12 and IFN-&#947; synergistically to the successive viral and pneumococcal challenge. Whereas prior influenza virus infection suppressed the IL-10 response independent of the timing of the subsequent pneumococcal stimulation.Conclusions: Our results demonstrated that successive challenge of dendritic cells with influenza virus and pneumococcus resulted in synergistic up-regulation of pro-inflammatory cytokines with simultaneous down-regulation of anti-inflammatory cytokine, which may explain the immuno-pathogenesis of this important co-infection. &#169; 2011 Wu et al; licensee BioMed Central Ltd.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine