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首页> 外文期刊>American Journal of Physiology >Surfactant dysfunction and lung injury due to the E. coli virulence factor hemolysin in a rat pneumonia model.
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Surfactant dysfunction and lung injury due to the E. coli virulence factor hemolysin in a rat pneumonia model.

机译：在大鼠肺炎模型中，由于大肠杆菌毒力因子溶血素引起的表面活性剂功能障碍和肺损伤。

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This study tests the hypothesis that the virulence factor hemolysin (Hly) expressed by extraintestinal pathogenic Escherichia coli contributes to surfactant dysfunction and lung injury in a rat model of gram-negative pneumonia. Rats were instilled intratracheally with CP9 (wild type, Hly-positive), CP9hlyA (Hly-minus), CP9/pEK50 (supraphysiological Hly), or purified LPS. At 6 h postinfection, rats given CP9 had a decreased percentage content of large surfactant aggregates in cell-free bronchoalveolar lavage (BAL), decreased large aggregate surface activity, decreased Pa(O2)/FiO2) ratio, increased BAL albumin/protein levels, and increased histological evidence of lung injury compared with rats given CP9hlyA or LPS. In addition, rats given CP9/pEK50 or CP9 had decreased large aggregate surface activity, decreased Pa(O2)/FiO2) ratios, and increased BAL albumin/protein levels at 2 h postinfection compared with rats given CP9hlyA. The severity of permeability lung injury based on albumin/protein levels in BAL at 2 h was ordered as CP9/pEK50 > CP9 > CP9hlyA > normal saline controls. Total lung titers of bacteria were increased at 6 h in rats given CP9 vs. CP9hlyA, but bacterial titers were not significantly different at 2 h, indicating that increased surfactant dysfunction and lung injury were associated with Hly as opposed to bacterial numbers per se. Further studies in vitro showed that CP9 could directly lyse transformed pulmonary epithelial cells (H441 cells) but that indirect lysis of H441 cells secondary to Hly-induced neutrophil lysis did not occur. Together, these data demonstrate that Hly is an important direct mediator of surfactant dysfunction and lung injury in gram-negative pneumonia.
机译：这项研究检验了以下假设：在革兰氏阴性肺炎大鼠模型中，肠外致病性大肠杆菌表达的毒力因子溶血素（Hly）导致表面活性剂功能障碍和肺损伤。大鼠气管内滴注CP9（野生型，Hly阳性），CP9hlyA（Hly减），CP9 / pEK50（超生理学Hly）或纯化的LPS。感染后6小时，给予CP9的大鼠在无细胞支气管肺泡灌洗液（BAL）中具有较大的表面活性剂聚集体百分比，降低了较大的聚集体表面活性，降低了Pa（O2）/ FiO2）比，增加了BAL白蛋白/蛋白质水平，与接受CP9hlyA或LPS的大鼠相比，肺损伤的组织学证据增加。此外，与使用CP9hlyA的大鼠相比，使用CP9 / pEK50或CP9的大鼠在感染后2 h的大骨料表面活性降低，Pa（O2）/ FiO2）比降低，BAL白蛋白/蛋白水平升高。根据CP2 / pEK50> CP9> CP9hlyA>生理盐水对照，按2小时BAL中白蛋白/蛋白水平对通透性肺损伤的严重程度进行排序。给予CP9和CP9hlyA的大鼠在6 h时细菌的总肺滴度增加，但在2 h时细菌滴度无显着差异，表明表面活性剂功能障碍和肺损伤与Hly相关，而不是细菌本身。体外进一步研究表明，CP9可以直接裂解转化的肺上皮细胞（H441细胞），但是继Hly诱导的中性粒细胞裂解后，H441细胞不会发生间接裂解。总之，这些数据表明，Hly是革兰氏阴性肺炎中表面活性剂功能障碍和肺损伤的重要直接介体。

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