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Article: Proinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cells

TitleProinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cells
Authors
KeywordsAvian
Chemokines
IP-10
Pathogenesis
Issue Date2005
PublisherBioMed Central Ltd. The Journal's web site is located at http://respiratory-research.com/
Citation
Respiratory Research, 2005, v. 6 How to Cite?
AbstractBackground: Fatal human respiratory disease associated with influenza A subtype H5N1 has been documented in Hong Kong, and more recently in Vietnam, Thailand and Cambodia. We previously demonstrated that patients with H5N1 disease had unusually high serum levels of IP-10 (interferon-gamma-inducible protein-10). Furthermore, when compared with human influenza virus subtype H1N1, the H5N1 viruses in 1997 (A/Hong Kong/483/97) (H5N1/97) were more potent inducers of pro-inflammatory cytokines (e.g. tumor necrosis factor-α) and chemokines (e.g. IP-10) from primary human macrophages in vitro, which suggests that cytokines dysregulation may play a role in pathogenesis of H5N1 disease. Since respiratory epithelial cells are the primary target cell for replication of influenza viruses, it is pertinent to investigate the cytokine induction profile of H5N1 viruses in these cells. Methods: We used quantitative RT-PCR and ELISA to compare the profile of cytokine and chemokine gene expression induced by H5N1 viruses A/HK/483/97 (H5N1/97), A/Vietnam/1194/04 and A/Vietnam/3046/04 (both H5N1/04) with that of human H1N1 virus in human primary alveolar and bronchial epithelial cells in vitro. Results: We demonstrated that in comparison to human H1N1 viruses, H5N1/97 and H5N1/04 viruses were more potent inducers of IP-10, interferon beta, RANTES (regulated on activation, normal T cell expressed and secreted) and interleukin 6 (IL-6) in primary human alveolar and bronchial epithelial cells in vitro. Recent H5N1 viruses from Vietnam (H5N1/04) appeared to be even more potent at inducing IP-10 than H5N1/97 virus. Conclusion: The H5N1/97 and H5N1/04 subtype influenza A viruses are more potent inducers of proinflammatory cytokines and chemokines in primary human respiratory epithelial cells than subtype H1N1 virus. We suggest that this hyper-induction of cytokines may be relevant to the pathogenesis of human H5N1 disease. © 2005 Chan et al., licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/44569
ISSN
2015 Impact Factor: 3.751
2015 SCImago Journal Rankings: 1.601
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, MCWen_HK
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorChui, WHen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorChan, YOen_HK
dc.contributor.authorChan, RWYen_HK
dc.contributor.authorLong, HTen_HK
dc.contributor.authorPoon, LLMen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.date.accessioned2007-10-30T06:04:33Z-
dc.date.available2007-10-30T06:04:33Z-
dc.date.issued2005en_HK
dc.identifier.citationRespiratory Research, 2005, v. 6en_HK
dc.identifier.issn1465-993Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/44569-
dc.description.abstractBackground: Fatal human respiratory disease associated with influenza A subtype H5N1 has been documented in Hong Kong, and more recently in Vietnam, Thailand and Cambodia. We previously demonstrated that patients with H5N1 disease had unusually high serum levels of IP-10 (interferon-gamma-inducible protein-10). Furthermore, when compared with human influenza virus subtype H1N1, the H5N1 viruses in 1997 (A/Hong Kong/483/97) (H5N1/97) were more potent inducers of pro-inflammatory cytokines (e.g. tumor necrosis factor-α) and chemokines (e.g. IP-10) from primary human macrophages in vitro, which suggests that cytokines dysregulation may play a role in pathogenesis of H5N1 disease. Since respiratory epithelial cells are the primary target cell for replication of influenza viruses, it is pertinent to investigate the cytokine induction profile of H5N1 viruses in these cells. Methods: We used quantitative RT-PCR and ELISA to compare the profile of cytokine and chemokine gene expression induced by H5N1 viruses A/HK/483/97 (H5N1/97), A/Vietnam/1194/04 and A/Vietnam/3046/04 (both H5N1/04) with that of human H1N1 virus in human primary alveolar and bronchial epithelial cells in vitro. Results: We demonstrated that in comparison to human H1N1 viruses, H5N1/97 and H5N1/04 viruses were more potent inducers of IP-10, interferon beta, RANTES (regulated on activation, normal T cell expressed and secreted) and interleukin 6 (IL-6) in primary human alveolar and bronchial epithelial cells in vitro. Recent H5N1 viruses from Vietnam (H5N1/04) appeared to be even more potent at inducing IP-10 than H5N1/97 virus. Conclusion: The H5N1/97 and H5N1/04 subtype influenza A viruses are more potent inducers of proinflammatory cytokines and chemokines in primary human respiratory epithelial cells than subtype H1N1 virus. We suggest that this hyper-induction of cytokines may be relevant to the pathogenesis of human H5N1 disease. © 2005 Chan et al., licensee BioMed Central Ltd.en_HK
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dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://respiratory-research.com/en_HK
dc.relation.ispartofRespiratory Researchen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAvianen_HK
dc.subjectChemokinesen_HK
dc.subjectIP-10en_HK
dc.subjectPathogenesisen_HK
dc.subject.meshBronchi - immunology - pathologyen_HK
dc.subject.meshCytokines - immunologyen_HK
dc.subject.meshInfluenza A Virus, H5N1 Subtype - immunologyen_HK
dc.subject.meshPulmonary Alveoli - immunologyen_HK
dc.subject.meshRespiratory Mucosa - immunology - pathologyen_HK
dc.titleProinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1465-9921&volume=6&spage=135&epage=&date=2005&atitle=Proinflammatory+cytokine+responses+induced+by+influenza+A+(H5N1)+viruses+in+primary+human+alveolar+and+bronchial+epithelial+cellsen_HK
dc.identifier.emailChan, MCW: mchan@hku.hken_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailTsao, GSW: gswtsao@hku.hken_HK
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hken_HK
dc.identifier.emailChan, RWY: reneewy@hku.hken_HK
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_HK
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.authorityChan, MCW=rp00420en_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.identifier.authorityChan, RWY=rp01596en_HK
dc.identifier.authorityPoon, LLM=rp00484en_HK
dc.identifier.authorityGuan, Y=rp00397en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1186/1465-9921-6-135en_HK
dc.identifier.pmid16283933en_HK
dc.identifier.pmcidPMC1318487en_HK
dc.identifier.scopuseid_2-s2.0-28044445881en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-28044445881&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.isiWOS:000234225700001-
dc.identifier.scopusauthoridChan, MCW=26654715500en_HK
dc.identifier.scopusauthoridCheung, CY=7202061836en_HK
dc.identifier.scopusauthoridChui, WH=7003524497en_HK
dc.identifier.scopusauthoridTsao, GSW=7102813116en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK
dc.identifier.scopusauthoridChan, YO=26667554300en_HK
dc.identifier.scopusauthoridChan, RWY=26661379100en_HK
dc.identifier.scopusauthoridLong, HT=7102434129en_HK
dc.identifier.scopusauthoridPoon, LLM=7005441747en_HK
dc.identifier.scopusauthoridGuan, Y=7202924055en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK

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