Keller G E, Dey R D, Burrell R
Department of Microbiology, University of Alabama, Birmingham.
Int Arch Allergy Appl Immunol. 1991;96(2):149-55. doi: 10.1159/000235486.
Endotoxin (lipopolysaccharide or LPS) inhalation has been implicated in increased pulmonary edema, most likely due to activation of an inflammatory response. The purpose of this study was to determine the cell types in the lung responsible for binding inhaled lipid A from Enterobacter agglomerans LPS. Five-hour exposures of aerosolized lipid A resulted in measurable pulmonary edema in hamsters, as determined by the accumulation of lung water. Immunocytochemistry was used to localize the inhaled lipid A in the cell types in the lung. Alveolar macrophages had decreased levels of lipid A as compared to unexposed controls, suggesting a possible metabolism by the macrophages. In vitro exposure of macrophages to lipid A resulted in a time-dependent clearance of lipid A which was inversely related to its concentration. Alveolar macrophages thus appear to be responsible for the removal of inhaled lipid A in this model and may initiate the physiological events which bring about pulmonary edema.
吸入内毒素（脂多糖或LPS）与肺水肿增加有关，最可能是由于炎症反应的激活。本研究的目的是确定肺部负责结合吸入的成团肠杆菌LPS中的脂质A的细胞类型。通过肺水的积聚确定，雾化脂质A暴露5小时导致仓鼠出现可测量的肺水肿。免疫细胞化学用于在肺细胞类型中定位吸入的脂质A。与未暴露的对照组相比，肺泡巨噬细胞中的脂质A水平降低，提示巨噬细胞可能对其进行了代谢。巨噬细胞在体外暴露于脂质A导致脂质A随时间清除，这与其浓度呈负相关。因此，在该模型中，肺泡巨噬细胞似乎负责清除吸入的脂质A，并可能引发导致肺水肿的生理事件。
