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
2011 Impact Factor: 3.118
2011 SCImago Journal Rankings: 0.263
DOIhttp://dx.doi.org/10.1186/1471-2334-11-201
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.

PubMed Central IDPMC3146832
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 Field
Value
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.grantControl of Pandemic and Inter-pandemic Influenza
dc.description.grantThe Role of Natural Killer Cells in the Pathogenesis of Avian Influenza Virus Infection
dc.description.grantcode97655
dc.description.grantcode98640
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
2011 Impact Factor: 3.118
2011 SCImago Journal Rankings: 0.263
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.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
Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine