Impact of cigarette smoke on clearance and inflammation after Pseudomonas aeruginosa infection
Impact of cigarette smoke on clearance and inflammation after Pseudomonas aeruginosa infection
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DOI：
10.1164/rccm.200311-1521oc
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发表时间：
2004-12-01
影响因子：
24.7
通讯作者：
Stämpfli, MR
中科院分区：
文献类型：
--
作者：
Drannik, AG;Pouladi, MA;Stämpfli, MR
本研究的目的是研究香烟烟雾对铜绿假单胞菌感染小鼠后细菌清除和免疫炎症参数的影响。我们观察到与假暴露小鼠相比，暴露于烟雾的小鼠的细菌清除率延迟。这与炎症增加有关，其特征是支气管肺泡灌洗液中的中性粒细胞和单核细胞数量增加。感染后，我们观察到与假暴露动物相比，烟雾暴露动物肺中促炎细胞因子（肿瘤坏死因子-α、白细胞介素-1 β和白细胞介素-6）和趋化因子（单核细胞趋化蛋白-1 [MCP-1]和巨噬细胞炎性蛋白-2 [MIP-2]）以及髓过氧化物酶和蛋白水解活性水平升高。延迟清除与吸烟小鼠的发病率增加和体重减轻有关。灭活细菌递送后，我们在烟雾暴露和假暴露的动物中观察到相似的炎症反应、临床评分和肿瘤坏死因子-α表达，表明炎症增加和临床表现改变是由于细菌清除率延迟。我们的研究结果表明，香烟烟雾会影响细菌引起的呼吸道免疫炎症反应。我们推测，改变呼吸道宿主防御可能与吸烟相关的疾病，如慢性阻塞性肺疾病。
The object of this study was to investigate the impact of cigarette smoke on bacterial clearance and immune inflammatory parameters after infection with Pseudomonas aeruginosa in mice. We observed a delayed rate of bacterial clearance in smoke-exposed compared with sham-exposed mice. This was associated with increased inflammation characterized by greater numbers of neutrophils and mononuclear cells in the bronchoalveolar lavage. After infection, we observed increased levels of proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6) and chemokines (monocyte chemoattractant protein-1 [MCP-1] and macrophage inflammatory protein-2 [MIP-2]) as well as myeloperoxidase and proteolytic activity in the lungs of smoke-exposed compared with sham-exposed animals. Delayed clearance was associated with increased morbidity and greater weight loss of smoke-exposed mice. After delivery of inactivated bacteria, we observed a similar inflammatory response, clinical score, and tumor necrosis factor-alpha expression in smoke- and sham-exposed animals, suggesting that increased inflammation and altered clinical presentation are due to the delayed rate of bacterial clearance. Our findings suggest that cigarette smoke affects respiratory immune-inflammatory responses elicited by bacteria. We postulate that altered respiratory host defense may be implicated in smoking-related diseases such as chronic obstructive pulmonary disease.