Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
J Innate Immun. 2010;2(2):96-106. doi: 10.1159/000243784. Epub 2009 Oct 1.
The pulmonary innate immune system has evolved over millions of years to provide swift detection of inhaled microbial agents and trigger well-balanced protective responses. Much more recent on the evolutionary scale is human activity, which has resulted in the release of a new class of potentially harmful, non-microbial compounds into the air. These xenobiotics include combustion by-products such as reactive oxygen species and polycyclic aromatic hydrocarbons. This review will summarize evidence showing how airborne xenobiotics can engage pulmonary innate immunity components at many levels. We will focus on potential effects of xenobiotics on airway dendritic cells, as these constitute key innate immune sensors in the lung, with the unique ability to initiate adaptive immunity. We propose that the aberrant processing of inhaled xenobiotics by an innate immune system that is now evolutionarily maladapted underlies the increase in chronic inflammatory lung diseases in modern times.
肺的先天免疫系统经过数百万年的进化，能够迅速检测到吸入的微生物，并引发平衡的保护反应。在进化的尺度上更近的是人类活动，这导致了一类新的潜在有害的非微生物化合物释放到空气中。这些外源性化学物质包括活性氧和多环芳烃等燃烧副产物。这篇综述将总结表明空气传播的外源性化学物质如何在多个层面上与肺先天免疫成分相互作用的证据。我们将重点关注外源性化学物质对气道树突状细胞的潜在影响，因为这些细胞构成了肺部先天免疫的关键传感器，具有启动适应性免疫的独特能力。我们提出，现在进化上不适应的先天免疫系统对吸入的外源性化学物质的异常处理，是导致现代慢性炎症性肺病增加的基础。
