Hypoxia, innate immunity and infection in the lung.

Hdl Handle:
http://hdl.handle.net/10147/207680
Title:
Hypoxia, innate immunity and infection in the lung.
Authors:
Schaible, Bettina; Schaffer, Kirsten; Taylor, Cormac T
Affiliation:
UCD Conway Institute, University College Dublin, Department of Microbiology, St. , Vincent's University Hospital, Dublin 4, Ireland.
Citation:
Respir Physiol Neurobiol. 2010 Dec 31;174(3):235-43. Epub 2010 Aug 13.
Journal:
Respiratory physiology & neurobiology
Issue Date:
1-Feb-2012
URI:
http://hdl.handle.net/10147/207680
DOI:
10.1016/j.resp.2010.08.006
PubMed ID:
20709192
Abstract:
The mucosal surface of the lung is the key interface between the external atmosphere and the bloodstream. Normally, this well oxygenated tissue is maintained in state of sterility by a number of innate immune processes. These include a physical and dynamic mucus barrier, the production of microbiocidal peptides and the expression of specific pattern recognition receptors on alveolar epithelial cells and resident macrophages and dendritic cells which recognise microbial structures and initiate innate immune responses which promote the clearance of potentially infectious agents. In a range of diseases, the mucosal surface of the lung experiences decreased oxygen tension leading to localised areas of prominent hypoxia which can impact upon innate immune and subsequent infectious and inflammatory processes. Under these conditions, the lung is generally more susceptible to infection and subsequent inflammation. In the current review, we will discuss recent data pertaining to the role of hypoxia in regulating both host and pathogen in the lung during pulmonary disease and how this contributes to innate immunity, infection and inflammation.
Language:
eng
MeSH:
Animals; Anoxia/*immunology/metabolism/pathology; Humans; *Immunity, Innate; Inflammation/immunology/metabolism/pathology; *Lung/metabolism/pathology/physiopathology; *Lung Diseases/immunology/metabolism/pathology; Oxygen/blood; Signal Transduction/physiology
ISSN:
1878-1519 (Electronic); 1569-9048 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorSchaible, Bettinaen_GB
dc.contributor.authorSchaffer, Kirstenen_GB
dc.contributor.authorTaylor, Cormac Ten_GB
dc.date.accessioned2012-02-01T10:34:46Z-
dc.date.available2012-02-01T10:34:46Z-
dc.date.issued2012-02-01T10:34:46Z-
dc.identifier.citationRespir Physiol Neurobiol. 2010 Dec 31;174(3):235-43. Epub 2010 Aug 13.en_GB
dc.identifier.issn1878-1519 (Electronic)en_GB
dc.identifier.issn1569-9048 (Linking)en_GB
dc.identifier.pmid20709192en_GB
dc.identifier.doi10.1016/j.resp.2010.08.006en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207680-
dc.description.abstractThe mucosal surface of the lung is the key interface between the external atmosphere and the bloodstream. Normally, this well oxygenated tissue is maintained in state of sterility by a number of innate immune processes. These include a physical and dynamic mucus barrier, the production of microbiocidal peptides and the expression of specific pattern recognition receptors on alveolar epithelial cells and resident macrophages and dendritic cells which recognise microbial structures and initiate innate immune responses which promote the clearance of potentially infectious agents. In a range of diseases, the mucosal surface of the lung experiences decreased oxygen tension leading to localised areas of prominent hypoxia which can impact upon innate immune and subsequent infectious and inflammatory processes. Under these conditions, the lung is generally more susceptible to infection and subsequent inflammation. In the current review, we will discuss recent data pertaining to the role of hypoxia in regulating both host and pathogen in the lung during pulmonary disease and how this contributes to innate immunity, infection and inflammation.en_GB
dc.language.isoengen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshAnoxia/*immunology/metabolism/pathologyen_GB
dc.subject.meshHumansen_GB
dc.subject.mesh*Immunity, Innateen_GB
dc.subject.meshInflammation/immunology/metabolism/pathologyen_GB
dc.subject.mesh*Lung/metabolism/pathology/physiopathologyen_GB
dc.subject.mesh*Lung Diseases/immunology/metabolism/pathologyen_GB
dc.subject.meshOxygen/blooden_GB
dc.subject.meshSignal Transduction/physiologyen_GB
dc.titleHypoxia, innate immunity and infection in the lung.en_GB
dc.contributor.departmentUCD Conway Institute, University College Dublin, Department of Microbiology, St. , Vincent's University Hospital, Dublin 4, Ireland.en_GB
dc.identifier.journalRespiratory physiology & neurobiologyen_GB
dc.description.provinceLeinster-

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