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目的和方法：选用正常大鼠肺泡巨噬细胞（ＡＭ），在高糖及高糖＋高胰岛素环境下培养，用卡介苗（ＢＣＧ）、干扰素ａ－２ｂ（ＩＦＮα－２ｂ）或两者联合活化，检测其贴壁率、四唑氮兰（ＮＢＴ）还原功能、ＮＯ和ＴＮＦ－α释放量并观察其超微结构改变。结果：高糖及高糖＋高胰岛素环境下活化ＡＭ贴壁延迟（Ｐ＜０．０１），ＮＢＴ还原功能明显被抑制（Ｐ＜０．０１）；ＢＣＧ和ＩＦＮα－２ｂ＋ＢＣＧ活化ＡＭ时，其ＮＯ和ＴＮＦα释放量均明显低于对照组（Ｐ＜０．０１）；ＩＦＮα－２ｂ活化ＡＭ时，其ＮＯ和ＴＮＦ－α释放量与对照组无明显差别（Ｐ＞０．０５）；细胞表面伪足减少、变短，胞质内高尔基氏体、粗面内质网减少。结论：在短期内高糖及高糖＋高胰岛素环境均抑制ＡＭ吞噬功能及改变超微结构，从而使糖尿病个体易发生肺部感染。
PURPOSE AND METHODS: Normal rat alveolar macrophages (AM) were selected and cultured in high glucose and high glucose + high insulin. BCG, IFNα-2b (IFNα-2b) or both The adherence rate, the reduction function of NBT, the release of NO and TNF-α were detected and their ultrastructural changes were observed. RESULTS: The delayed adhesion of activated AMs in high glucose and high glucose + high insulin groups was delayed (P <0.01), and the NBT reduction was significantly inhibited (P <0.01). When AM was stimulated with BCG and IFNα-2b + (P <0.01). The release of NO and TNF-α in IFN-α-2b was not significantly different from that in control group (P> 0.05). The cell surface fake Foot reduction, shortening, cytoplasmic Golgi apparatus, rough endoplasmic reticulum reduced. Conclusion: In the short-term, high glucose, high glucose and high insulin inhibited the phagocytosis of AM and changed the ultrastructure so that individuals with diabetes were prone to develop pulmonary infection.