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目的 :通过博莱霉素致大鼠肺纤维化过程中肺泡巨噬细胞表面白细胞粘附分子 CD11b,CD18及相应配体 CD5 4表达的动态观察 ,研究白细胞粘附分子对肺泡炎的触发作用。方法 :采用流式细胞仪和免疫组化方法。结果 :肺泡巨噬细胞 CD11b,CD18的表达在博莱霉素灌注后 1d即开始增高 ,7～ 14d天达高峰 ,与对照组差异显著(P <0 .0 0 1) ,随后略下降 ,但仍处于高水平表达。而 CD5 4在 3d后表达明显升高 ,以后呈持续性高水平表达。且7d时 CD11b,CD5 4的表达与 BAL F中的肺泡巨噬细胞 (Alveolar macrophage,AM)的数量呈正相关 ,γ值分别为0 .995 ,0 .885。两周后 BAL F中的肺泡巨噬细胞数量恢复正常 ,而其表面 CD11b,CD18,CD5 4的表达仍然增强。结论 :博莱霉素致大鼠肺纤维化发生机制中 CD11b,CD18,CD5 4表达增强 ,其在触发肺泡炎症及介导肺纤维化过程中起一定的作用。
OBJECTIVE: To investigate the leukocyte adhesion molecule-triggered triggering of alveolitis by observing the expression of leukocyte adhesion molecules CD11b, CD18 and CD54 on the surface of alveolar macrophages during bleomycin-induced pulmonary fibrosis in rats. Methods: Flow cytometry and immunohistochemistry were used. Results: The expression of CD11b and CD18 in alveolar macrophages began to increase at 1 day after bleomycin infusion and peaked at 7 to 14 days (P <0.01), then decreased slightly Still at a high level of expression. However, the expression of CD5 4 increased significantly after 3d and showed persistent high level expression afterwards. The expression of CD11b and CD54 on 7d was positively correlated with the number of Alveolar macrophage (AM) in BALF, with the values of γ = 0.995 and 0.885. After two weeks, the number of alveolar macrophages in BALF returned to normal while the expression of CD11b, CD18 and CD54 on the surface of BALF was still increased. Conclusion: The expression of CD11b, CD18 and CD54 in bleomycin-induced pulmonary fibrosis in rats is increased, which plays a role in triggering alveolar inflammation and mediating pulmonary fibrosis.