肺炎克雷伯杆菌肺炎老龄大鼠心肌损伤中TNF-αIL-1及MIP-2表达的意义

Changes of TNF-α,IL-1,MIP-2 in the aged rats' heart injury with Klebsiella pneumonia

目的从心肌组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、巨噬细胞炎症蛋白-2(MIP-2)的表达和MIP-2 mRNA表达变化揭示老年肺炎导致心肌损伤的病理机制。方法复制肺炎克雷伯杆菌肺炎模型,大鼠分为青龄对照组、青龄模型组、老龄对照组、老龄模型组。观察肺脏和心脏的普通病理改变及心肌组织的超微结构,计数外周血和肺泡灌洗液白细胞及中性粒细胞,采用免疫组织化学方法和原位杂交方法测定心肌组织TNF-α、IL-1、MIP-2蛋白表达和MIP-2 mRNA表达。结果老龄模型组的肺脏损伤、心肌损伤和肺脏细菌计数的增高较青龄模型组严重。青龄模型组和老龄模型组外周血和肺泡灌洗液白细胞和中性粒细胞分别高于青龄对照组和老龄对照组。青龄模型组和老龄模型组心肌组织TNF-α、IL-1、MIP-2蛋白表达和MIP-2 mRNA表达分别较青龄对照组和老龄对照组增强,老龄对照组的表达均弱于青龄对照组,老龄模型组的表达均较青龄模型组增强。结论细胞因子TNF-α和IL-1及MIP-2表达增强参与肺炎导致心肌损伤的发生,这些因子的过度表达可能是老年肺炎导致心肌损伤严重的部分机制。

Objective To study the heart injury pathophysiological characters of pneumonia by the changes of TNF - α, IL - 1, MIP - 2 in the aged rats＇ cardiac muscle. Methods The model of rats with Klebsiella pneumonia were duplicated and the rats were divided into young control group （YCG ） , young model group（ YMG） ,aged control group（ ACG） and aged model group（ AMG）. It was observed that the pathological change of lung tissue and cardiac muscle by light microscope and electron microscope, and the count of neutrophil in peripheral blood and bronchoalveolar lavage fluid （ BALF） , count the changes of TNF-α ,IL- 1 ,MIP- 2, MIP- 2 mRNA in the aged rats＇ cardiac muscle by immunohistochemistry and hybridization in situ. Results The lung tissue injury, myocardial damage and lung＇s bacterial count in the AMG were higher than that in the YMG. The count of leukocyte and neutrophil in peripheral blood and BALF in the YMG and AMG was higher than that in the YCG and ACC. The count of TNF - α, IL - 1, MIP - 2 in the cardiac muscle were higher in the YMG and the AMG than those in the YCG and the ACC. The count of TNF - α,IL - 1 ,MIP - 2 in the cardiac muscle were lower in the ACG than those in the YCG. The count of TNF - α, IL - 1, MIP - 2 in the cardiac muscle were higher in the AMG than those in the YMG. Conclusions The overexpression of TNF - α, IL - 1, MIP - 2 was participated the myocardial damage induced by pneumonia. The overexpression of those cytokines maybe the mechanisms of the severe myocardial damage induced by pneumonia.