Herr C, Beisswenger C, Hess C, Kandler K, Suttorp N, Welte T, Schroeder J-M, Vogelmeier C
Department of Internal Medicine, Division of Pulmonology, Hospital of the University of Marburg, Baldingerstrasse 1, 35043 Marburg, Germany.
Thorax. 2009 Feb;64(2):144-9. doi: 10.1136/thx.2008.102681. Epub 2008 Oct 13.
Smoking increases the susceptibility to pulmonary infection and is a risk factor for the development of chronic obstructive pulmonary disease (COPD). It is postulated that cigarette smoke suppresses the activation of the innate immune system in response to bacterial infection.
Using sensitive ex vivo analysis, the level of the endogenous antibiotic peptide human beta-defensin-2 (hBD-2) was measured in pharyngeal washing fluid and sputum from patients with community acquired pneumonia. The regulation of antibacterial host defence molecules was studied in vitro. The effect of cigarette smoke on the antibacterial activity of differentiated airway epithelium and the expression of host defence molecules was studied in an in vitro infection model.
Current or former smoking was associated with significantly reduced hBD-2 levels in pharyngeal washing fluid and sputum from patients with acute pneumonia. Exposure of airway epithelium to smoke in vitro inhibited the induction of hBD-2 by bacteria. This correlated with decreased antimicrobial activity. This effect was mimicked by hydrogen peroxide, and catalase blunted the smoke-induced inhibition of epithelial host defence.
Smoke exposure suppresses the induction of epithelial antibacterial host defences. These findings link smoking with increased susceptibility to infection. This mechanism may be important in the pathogenesis of pneumonia and COPD.
吸烟会增加肺部感染的易感性，是慢性阻塞性肺疾病（COPD）发生的一个危险因素。据推测，香烟烟雾会抑制机体针对细菌感染的固有免疫系统激活。
采用灵敏的体外分析方法，检测社区获得性肺炎患者咽洗液和痰液中内源性抗菌肽人β-防御素-2（hBD-2）的水平。在体外研究抗菌宿主防御分子的调控情况。在体外感染模型中研究香烟烟雾对分化气道上皮抗菌活性及宿主防御分子表达的影响。
目前或既往吸烟与急性肺炎患者咽洗液和痰液中hBD-2水平显著降低相关。体外将气道上皮暴露于烟雾中会抑制细菌诱导的hBD-2产生。这与抗菌活性降低相关。过氧化氢可模拟此效应，而过氧化氢酶可减弱烟雾诱导的上皮宿主防御抑制作用。
暴露于烟雾会抑制上皮抗菌宿主防御的诱导。这些发现将吸烟与感染易感性增加联系起来。该机制可能在肺炎和COPD的发病机制中起重要作用。
