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首页> 外文期刊>American Journal of Physiology >Cigarette smoke exposure worsens acute lung injury in antibiotic-treated bacterial pneumonia in mice
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Cigarette smoke exposure worsens acute lung injury in antibiotic-treated bacterial pneumonia in mice

机译：香烟烟雾暴露在小鼠中抗生素治疗的细菌肺炎恶化急性肺损

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Evidence is accumulating that exposure to cigarette smoke (CS) increases the risk of developing acute respiratory distress syndrome (ARDS). Streptococcus pneumoniae is the most common cause of bacterial pneumonia, which in turn is the leading cause of ARDS. Chronic smokers have increased rates of pneumo-coccal colonization and develop more severe pneumococcal pneumonia than nonsmokers; yet mechanistic connections between CS exposure, bacterial pneumonia, and ARDS pathogenesis remain relatively unexplored. We exposed mice to 3 wk of moderate whole body CS or air, followed by intranasal inoculation with an invasive serotype of S. pneumoniae. CS exposure alone caused no detectable lung injury or bronchoalveolar lavage (BAL) inflammation. During pneumococcal infection, CS-exposed mice had greater survival than air-exposed mice, in association with reduced systemic spread of bacteria from the lungs. However, when mice were treated with antibiotics after infection to improve clinical relevance, the survival benefit was lost, and CS-exposed mice had more pulmonary edema, increased numbers of BAL monocytes, and elevated monocyte and lymphocyte chemo-kines. CS-exposed antibiotic-treated mice also had higher serum surfactant protein D and angiopoietin-2, consistent with more severe lung epithelial and endothelial injury. The results indicate that acute CS exposure enhances the recruitment of immune cells to the lung during bacterial pneumonia, an effect that may provide microbiological benefit but simultaneously exposes the mice to more severe inflammatory lung injury. The inclusion of antibiotic treatment in preclinical studies of acute lung injury in bacterial pneumonia may enhance clinical relevance, particularly for future studies of current or emerging tobacco products.
机译：证据积累了卷烟烟雾（CS）的暴露增加了发育急性呼吸窘迫综合征（ARDS）的风险。肺炎链球菌是细菌肺炎最常见的原因，这反过来是ARDS的主要原因。慢性吸烟者增加了肺炎群殖民殖民的速率，并且比非闻名者培养更严重的肺炎球菌;然而，Cs暴露，细菌肺炎和ARDS发病机构之间的机械连接仍然是相对未开发的。我们将小鼠暴露于3周的中度全身Cs或空气，然后用鼻内接种，血管型血管型。 CS暴露单独导致无可检测的肺损伤或支气管肺泡灌洗（BAL）炎症。在肺炎球菌感染期间，CS暴露的小鼠比空气暴露的小鼠的存活更大，与肺部的细菌的系统蔓延减少。然而，当感染后用抗生素治疗小鼠以改善临床相关性时，生存效果丢失，并且CS暴露的小鼠具有更多的肺水肿，增加的BAL单核细胞数，单核细胞和淋巴细胞和淋巴细胞化疗升高。暴露的抗生素治疗的小鼠还具有更高的血清表面活性剂蛋白D和血管发成素-2，与更严重的肺上皮和内皮损伤一致。结果表明，急性Cs暴露在细菌肺炎期间增强免疫细胞对肺的募集，这是一种可以提供微生物效益，但同时使小鼠暴露于更严重的炎症肺损伤。在细菌肺炎急性肺损伤的临床前研究中包含抗生素治疗可能提高临床相关性，特别是对于对当前或新兴烟草产品的未来研究。

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