Hypoxia, innate immunity and infection in the lung
|Title:||Hypoxia, innate immunity and infection in the lung||Authors:||Schaible, Bettina
Taylor, Cormac T.
|Permanent link:||http://hdl.handle.net/10197/5583||Date:||Dec-2010||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.||Type of material:||Journal Article||Publisher:||Elsevier||Copyright (published version):||2010 Elsevier||Keywords:||Lung;Hypoxia;Innate immunity;Inflammation;Pulmonary disease||DOI:||10.1016/j.resp.2010.08.006||Language:||en||Status of Item:||Peer reviewed|
|Appears in Collections:||Conway Institute Research Collection|
SBI Research Collection
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