UCD Conway Institute, University College Dublin, Department of Microbiology, St. Vincent’s University Hospital, Dublin 4, Ireland.
Respir Physiol Neurobiol. 2010 Dec 31;174(3):235-43. doi: 10.1016/j.resp.2010.08.006. Epub 2010 Aug 13.
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.
肺部的黏膜表面是外部大气与血液之间的关键界面。通常，通过多种先天免疫过程，这个富含氧气的组织可以保持无菌状态。这些过程包括物理和动态的黏液屏障、杀菌肽的产生，以及肺泡上皮细胞和驻留巨噬细胞和树突状细胞上特定模式识别受体的表达，这些受体可以识别微生物结构并启动先天免疫反应，从而促进潜在感染因子的清除。在一系列疾病中，肺部的黏膜表面会经历氧气张力下降，导致局部明显缺氧，这可能会影响先天免疫以及随后的感染和炎症过程。在这些情况下，肺部通常更容易受到感染和随后的炎症的影响。在本综述中，我们将讨论最近有关缺氧在肺部疾病期间调节宿主和病原体的作用的数据，以及这如何促进先天免疫、感染和炎症。
