Altered lung function relates to inflammation in an acute LPS mouse model
Altered lung function relates to inflammation in an acute LPS mouse model
复制标题
DOI：
10.1016/j.pupt.2012.08.001
复制
发表时间：
2012-10-01
影响因子：
3.2
通讯作者：
Lal, Harbans
中科院分区：
文献类型：
--
作者：
Hakansson, Hanna Falk;Smailagic, Amir;Lal, Harbans
脂多糖（LPS）诱导的急性肺损伤的临床前体内模型通常用于概括慢性阻塞性肺疾病和急性加重的病理生理特征。LPS诱导的肺部炎症是很好的描述，但是，是否炎性反应涉及时间特异性肺功能的改变还没有阐明。在相应时间点进行支气管肺泡灌洗液中炎性细胞和炎性介质的定量以及无创和有创肺功能测定。LPS诱导的肺组织病理学改变明显，48 h时肺内炎性细胞浸润达到高峰。在该时间点，观察到炎症介质显著增加，肺容量和力学参数显著改变。布地奈德可预防LPS诱导的肺部炎症和肺功能障碍，这些结果表明炎性细胞流入峰值与肺功能显著损害之间存在时间关系，提示炎症的致病作用。这些结果使我们更好地理解呼吸系统疾病中肺部炎症的功能后果。(C)2012爱思唯尔有限公司版权所有。
Preclinical in vivo models of lipopolysaccharide (LPS)-induced acute lung injury are commonly used to recapitulate pathophysiological features of chronic obstructive pulmonary disease and acute exacerbations. The LPS-induced lung inflammation is well described; however, whether the inflammatory response relates temporally to specific alterations in lung function has not been elucidated.We have investigated the effects of acute LPS inhalation in mice up to 96 h post LPS. Quantitation of inflammatory cells and inflammatory mediators in bronchoalveolar lavage fluid and non-invasive and invasive lung function measurements were performed at corresponding time points. The inhibitory effect of the glucocorticoid, budesonide, on LPS-induced lung inflammation and lung function was determined.LPS inhalation induced distinct histopathological changes, and infiltration of inflammatory cells to the lungs peaked at 48 h. At this time point, significantly increased inflammatory mediators and significantly altered lung capacity and mechanics parameters were observed. Budesonide given per os prevented the LPS-induced lung inflammation and lung dysfunction.These results demonstrate a temporal relationship between the peak of inflammatory cell influx and significant impairment of lung function, suggestive of a causative role of inflammation. These results allow better understanding of the functional consequences of lung inflammation in respiratory diseases. (C) 2012 Elsevier Ltd. All rights reserved.