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Article: Report of the 'Mechanisms of lung injury and immunomodulator interventions in influenza' workshop, 21 March 2010, Ventura, California, USA

TitleReport of the 'Mechanisms of lung injury and immunomodulator interventions in influenza' workshop, 21 March 2010, Ventura, California, USA
Authors
Issue Date2011
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/subs.asp?ref=1750-2640&site=1
Citation
Influenza And Other Respiratory Viruses, 2011, v. 5 n. 6, p. 453-e475 How to Cite?
AbstractThe clinical course of influenza and the extent of lung injury are determined by both viral and host factors, as well as sometimes secondary bacterial infections and exacerbations of underlying conditions. The balance between viral replication and the host immune responses is central to disease pathogenesis, and the extent of lung injury in severe influenza infections may be due in part to overly exuberant or dysregulated innate inflammatory responses or sometimes deficient responses. Acute respiratory distress syndrome (ARDS) is the principal cause of respiratory failure associated with severe influenza. ARDS can be triggered by both direct lung insults (e.g. respiratory pathogens) and systemic insults (e.g. sepsis), and the lung damage is exacerbated by the inflammatory response associated with either infectious or non-infectious insults. This workshop aimed to review the current understanding of lung injury in acute influenza and describe cellular and molecular mechanisms of lung injury that are common to influenza and infections by other respiratory pathogens. In addition, therapeutic agents that target host response proteins and pathways were identified and investigational agents in development reviewed. A logical strategy would be to combine antiviral treatment with drugs that modify excessive host responses or supplement deficient ones. However, a better understanding of common cell signalling pathways associated with acute lung injury caused by influenza and other pathogens is necessary to understand immunopathologic causes of lung injury. This will help determine which immunomodulatory interventions might be useful, and to predict the appropriate timing and consequences of their use. © 2011 Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/179831
ISSN
2015 Impact Factor: 2.378
2015 SCImago Journal Rankings: 1.570
References

 

DC FieldValueLanguage
dc.contributor.authorHoward, WAen_US
dc.contributor.authorPeiris, Men_US
dc.contributor.authorHayden, FGen_US
dc.date.accessioned2012-12-19T10:05:16Z-
dc.date.available2012-12-19T10:05:16Z-
dc.date.issued2011en_US
dc.identifier.citationInfluenza And Other Respiratory Viruses, 2011, v. 5 n. 6, p. 453-e475en_US
dc.identifier.issn1750-2640en_US
dc.identifier.urihttp://hdl.handle.net/10722/179831-
dc.description.abstractThe clinical course of influenza and the extent of lung injury are determined by both viral and host factors, as well as sometimes secondary bacterial infections and exacerbations of underlying conditions. The balance between viral replication and the host immune responses is central to disease pathogenesis, and the extent of lung injury in severe influenza infections may be due in part to overly exuberant or dysregulated innate inflammatory responses or sometimes deficient responses. Acute respiratory distress syndrome (ARDS) is the principal cause of respiratory failure associated with severe influenza. ARDS can be triggered by both direct lung insults (e.g. respiratory pathogens) and systemic insults (e.g. sepsis), and the lung damage is exacerbated by the inflammatory response associated with either infectious or non-infectious insults. This workshop aimed to review the current understanding of lung injury in acute influenza and describe cellular and molecular mechanisms of lung injury that are common to influenza and infections by other respiratory pathogens. In addition, therapeutic agents that target host response proteins and pathways were identified and investigational agents in development reviewed. A logical strategy would be to combine antiviral treatment with drugs that modify excessive host responses or supplement deficient ones. However, a better understanding of common cell signalling pathways associated with acute lung injury caused by influenza and other pathogens is necessary to understand immunopathologic causes of lung injury. This will help determine which immunomodulatory interventions might be useful, and to predict the appropriate timing and consequences of their use. © 2011 Blackwell Publishing Ltd.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/subs.asp?ref=1750-2640&site=1en_US
dc.relation.ispartofInfluenza and other Respiratory Virusesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunologic Factors - Therapeutic Useen_US
dc.subject.meshInfluenza A Virus, H1n1 Subtype - Genetics - Immunology - Physiologyen_US
dc.subject.meshInfluenza A Virus, H5n1 Subtype - Genetics - Immunology - Physiologyen_US
dc.subject.meshInfluenza, Human - Complications - Immunology - Virologyen_US
dc.subject.meshLung Injury - Drug Therapy - Etiology - Immunologyen_US
dc.titleReport of the 'Mechanisms of lung injury and immunomodulator interventions in influenza' workshop, 21 March 2010, Ventura, California, USAen_US
dc.typeArticleen_US
dc.identifier.emailPeiris, M: malik@hkucc.hku.hken_US
dc.identifier.authorityPeiris, M=rp00410en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1750-2659.2011.00278.xen_US
dc.identifier.pmid21848616-
dc.identifier.scopuseid_2-s2.0-80054791083en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80054791083&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume5en_US
dc.identifier.issue6en_US
dc.identifier.spage453en_US
dc.identifier.epagee475en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridHoward, WA=7202832152en_US
dc.identifier.scopusauthoridPeiris, M=7005486823en_US
dc.identifier.scopusauthoridHayden, FG=7103233446en_US

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