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目的:比较研究HIV病毒包膜蛋白gp120与卡介苗分别及共同感染人巨噬细胞,对人巨噬细胞的破坏能力及诱导巨噬细胞产生一氧化氮(NO)能力的差异性。方法:gp120与卡介苗(BCG)分别及共同感染人巨噬细胞后,于不同时间点采用MTT法检测巨噬细胞存活率,利用硝酸还原酶法检测细胞培养上清液中NO的含量。结果:gp120与BCG分别及共同感染人巨噬细胞,均可降低巨噬细胞的存活率,但gp120与卡介苗共同感染巨噬细胞,其存活率降低更为显著(P<0.05);gp120与BCG均可激活人巨噬细胞合成和释放NO,而gp120与BCG共同感染组激活人巨噬细胞合成和释放NO的量明显低于BCG感染组(P<0.05)。结论:gp120感染巨噬细胞可影响巨噬细胞抗微生物的活性,可增强卡介苗对巨噬细胞的破坏作用。
OBJECTIVE: To comparatively study the difference of HIV-1 envelope protein gp120 and BCG in co-infecting human macrophages, their ability to destroy human macrophages and the ability of inducing macrophages to produce nitric oxide (NO). Methods: After the macrophages were infected with BCG and gp120 respectively, the survival rate of macrophages was detected by MTT assay at different time points. The content of NO in cell culture supernatant was detected by nitrate reductase method. Results: Both gp120 and BCG co-infected macrophages and macrophages could reduce the survival rate of macrophages. However, gp120 co-infected with BCG significantly decreased the survival rate of macrophages (P <0.05) Both activated human macrophages to synthesize and release NO. However, the amount of NO synthesized and activated by human macrophages co-infected with gp120 and BCG was significantly lower than that of BCG-infected cells (P <0.05). CONCLUSION: Macrophages infected with gp120 can affect the antimicrobial activity of macrophages and enhance the destructive effect of BCG on macrophages.