严重胸部创伤对肺泡及间质巨噬细胞MHC-Ⅱ表达的影响

Effect of severe thoracic trauma combining endotoxin infection on MHC-Ⅱexpression of alveolar macrophages and pulmonary interstitial macrophages

目的 观察严重胸部创伤后肺泡(AM)及间质(IM)巨噬细胞两类亚群MHC Ⅱ表达的不同变化,并探讨其意义。方法 建立严重胸部创伤模型,支气管肺泡灌洗,机械结合酶消化法分离、培养肺泡及间质巨噬细胞,动态检测创伤前、创伤后2、4、8、16、2 4h以及复合LPS攻击后肺泡及间质巨噬细胞MHC Ⅱ的表达水平。结果 利用小型多功能生物撞击机以4 0 0kPa驱动压力对大鼠右侧上胸壁进行致伤,能够建立稳定可靠并符合临床特点的严重胸部创伤模型;IM的MHC Ⅱ表达强于AM ,创伤复合脂多糖(LPS)刺激能抑制它们的MHC Ⅱ表达,AM在伤后4h最低,伤后2 4h恢复正常,IM在伤后8h即恢复正常并持续增高。结论 严重胸部创伤对AM、IM的MHC Ⅱ表达具有不同影响,它们在创伤后机体免疫功能紊乱的过程中具有不同作用,本研究为创伤性急性肺损伤的发病机制提供了一定的实验及理论依据。

Objective To observe the different changes of antigen presentation of alveolar macrophages (AMs) and interstitial ma- crophages (IMs) after severe thoracic trauma. Methods For establishing a rat model of severe thoracic trauma, the alveolar macrophages were collected by the bronchoalveolar lavage fluid, mechanic flush, and enzymatic digestion, and then were separated and cultured. The antigen presentation of AM and IM were observed dynamically before and after trauma. Results A stable and reliable severe thoracic trauma model was successfully established with 400 kPa-strike on the up-right chest of rat by a multiple-function strike apparatus. The antigen presentation of IM was stronger than that of AM, and trauma with LPS challenge could inhibit this function in both AM and IM. The lowest MHC-Ⅱexpression of AMs occurred at 4 h posttrauma, recovered at 24 h posttrauma, and that of IMs recovered at 8 h pottrauma and kept up-regulation. Conclu- sion There is different process in immune function turbulence between AM and IM. The results provide valuable laboratorial and theoretical evidence for the research on ALI complicated with severe thoracic trauma.