Suppression of mycobacterium tuberculosis induced reactive oxygen species and tumor necrosis factor-alpha activity in human monocytes of systemic lupus erythematosus patients by reduced glutathione.
Suppression of mycobacterium tuberculosis induced reactive oxygen species and tumor necrosis factor-alpha activity in human monocytes of systemic lupus erythematosus patients by reduced glutathione.
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DOI：
10.5001/omj.2012.03
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发表时间：
2012-01-01
影响因子：
--
通讯作者：
Islam, Najmul
中科院分区：
文献类型：
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作者：
Azfar, Shah Farhan;Islam, Najmul
目的：系统性红斑狼疮的病因和发病机制尚不清楚，有证据表明与分支杆菌抗原有关。方法：将100例SLE患者分为SLE组（n=30）、TB组（n = 30）、SLE-TB组（n = 30）和对照组（n=10），观察结核分枝杆菌感染对SLE患者临床病程的影响，以及ROS和TNF-α在结核病相关SLE患者发病机制中的作用。结果：SLE组和SLE-TB组均以发热、关节炎、皮疹、光敏反应等为主要临床表现，SLE组和SLE-TB组均以发热、关节炎、皮疹、光敏反应等为主要临床表现。还原型谷胱甘肽表现出改善活性氧和肿瘤坏死因子-α诱导的行动，这反过来又抑制了免疫结合观察到的结核病和SLE患者培养无glutathione.CONCLUSION：数据显示，SLE患者更容易发展结核分枝杆菌，作为活性氧和肿瘤坏死因子-α在SLE患者可以激活复制的分枝杆菌Ag 85 B（30 kDa）后，杆菌感染。
OBJECTIVES: The etiology and pathogenesis of systemic lupus erythematosus remains unknown, evidence exists for the involvement of mycobacterial antigen. This study is aimed to determine the effect of Mycobacterium tuberculosis on clinical course of SLE patients and the role of ROS and TNF-alpha in the pathogenesis of tuberculosis associated SLE patients.METHODS: This study was done on 100 patients divided into SLE group (n=30), TB group (n=30), SLE-TB group (n=30) and control group (n=10). All patients underwent clinical, biochemical and immunological evaluation by employing techniques such as SDS-PAGE, direct binding and competition ELISA, PBMC and cell culture.RESULTS: Fever, arthritis, skin rash, photosensitivity were more common in both SLE and SLE-TB group. Reduced glutathione showed amelioration of ROS and TNF-alpha induced action, which in turn, subsequently suppressed the immune-bindings observed in monocytes of TB and SLE patients cultured without glutathione.CONCLUSION: Data shows that SLE patients are more susceptible to developing Mycobacterium tuberculosis, as ROS and TNF-alpha in SLE patients could activate the replication of mycobacterial Ag85B (30 kDa) after bacilli infection.