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从正常Ｗｉｓｔａｒ大鼠肺中分离出肺泡巨噬细胞，在体外正常和高糖状态下培养并分别以干扰素（ＩＦＮａ－２ｂ、卡介苗（ＢＣＧ）以及干扰素和卡介苗联合刺激肺泡巨噬细胞，测定其释放一氧化氮（ＮＯ）和肿瘤坏死因子－ａ（ＴＮＦ－ａ）量。结果显示，高糖状态下ＢＣＧ刺激肺泡巨噬细胞时。其ＮＯ和ＴＮＦ－ａ释放量明显低于对照组（Ｐ＜０．０１）：ＩＦＮａ－２ｂ刺激肺泡巨噬细胞时，其ＮＯ和ＴＮＦ－ａ释放量与对照组无差别（Ｐ＞０．０５）：ＩＦＮａ－２ｂ与ＢＣＧ协同刺激肺泡巨噬细胞时，其ＮＯ和ＴＮＦ－ａ释放量明显低于对照组（Ｐ＜０．０１）。由此表明高糖状态下。肺泡巨噬细胞释放ＮＯ和ＴＮＦ－ａ减少，可能是导致糖尿病患者肺部易感染的一个重要原因。
Alveolar macrophages were isolated from the lungs of normal Wistar rats and cultured in vitro under normal and high glucose conditions and stimulated alveolar macrophages with interferon (IFNa-2b, BCG, interferon and BCG respectively) The release of nitric oxide (NO) and tumor necrosis factor-a (TNF-a) showed that the release of NO and TNF-α in BCG-stimulated alveolar macrophages under high glucose condition was significantly lower than that of the control group P <0.01): When IFNα-2b stimulated alveolar macrophages, the release of NO and TNF-α did not differ from that of the control group (P> 0.05). When IFNα-2b and BCG synergistically stimulated alveolar macrophages , The release of NO and TNF-a were significantly lower than those of the control group (P <0.01), which indicated that the release of NO and TNF-α from alveolar macrophages in high glucose condition may be the cause of lung damage in diabetic patients An important reason for infection.