巨噬细胞炎症蛋白—2在内毒素性急性肺损伤中的作用

目的：探讨巨噬细胞炎症蛋白２（ＭＩＰ２）在内毒素性急性肺损伤（ＡＬＩ）中的可能作用。方法：采用斑点杂交及原位杂交技术对ＡＬＩ大鼠肺组织中ＭＩＰ２ｍＲＮＡ的表达进行定量和定位研究。结果：内毒素性ＡＬＩ时大鼠各时点肺组织ＭＩＰ２ｍＲＮＡ表达量显著高于对照组，且与血浆及肺组织匀浆髓过氧化酶（ＭＰＯ）活性呈正相关（ｒ＝０．７２９，０．８８５，Ｐ均＜０．０５）。原位杂交发现，在ＡＬＩ早期，肺内巨噬细胞是ＭＩＰ２的主要分泌细胞。结论：在ＡＬＩ早期，巨噬细胞释放的ＭＩＰ２可能是ＡＬＩ时多形核白细胞（ＰＭＮ）在肺内大量浸润并激活的原因之一。

The potential role of chemokine macrophage inflammatory protein2 in endotoxininduced acute lung injury

Objective:To explore the potential role of chemokine macrophage inflammatory protein2 (MIP2) in endotoxininduced acute lung injury (ALI).Methods:By dot hybridization and in situ hybridization techniques,the quantity and distribution of MIP2 mRNA in endotoxininduced ALI were investigated.Results:The expression of pulmonary MIP2 mRNA in animals subjected to endotoxininduced ALI was markedly higher than those in the control group (all P <0 01),and MIP2 mRNA levels were positively correlated to myeloperoxidase (MPO) activities both in plasma and pulmonary tissue ( r =0 729,0 885,both P <0 05).By in situ hybridization method,it was found that the pulmonary macrophages were the predominant cell sources of MIP2 at the early stage of ALI.Conclusions:MIP2 released mainly by alveolar macrophage might contribute to the sequestration and activation of polymorphonuclear neutrophil leukocytes (PMN) in the lungs associated with endotoxin challenge,and it plays a role in the pathogenesis of ALI.