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Hypoxia, innate immunity and infection in the lung
Date Issued
2010-12
Date Available
2014-05-02T09:12:00Z
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
Journal
Respiratory Physiology & Neurobiology
Volume
174
Issue
3
Start Page
235
End Page
243
Copyright (Published Version)
2010 Elsevier
Language
English
Status of Item
Peer reviewed
This item is made available under a Creative Commons License
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