Glutathione and growth inhibition of Mycobacterium tuberculosis in healthy and HIV infected subjects

被引:33
作者
Venketaraman V. [1 ,2 ,3 ,4 ,5 ,6 ]
Rodgers T. [1 ,4 ,6 ]
Linares R. [6 ]
Reilly N. [1 ,4 ,6 ]
Swaminathan S. [1 ,4 ,6 ]
Hom D. [2 ,6 ]
Millman A.C. [1 ,4 ,6 ]
Wallis R. [1 ,4 ,6 ,7 ]
Connell N.D. [1 ,2 ,3 ,4 ,5 ,6 ]
机构
[1] Division of Infectious Diseases, UMDNJ-New Jersey Medical School, Newark
[2] Center for Emerging and Re-Emerging Pathogens, UMDNJ-New Jersey Medical School, Newark
[3] National Tuberculosis Center, UMDNJ-New Jersey Medical School, Newark
[4] Department of Medicine, UMDNJ-New Jersey Medical School, Newark
[5] Department of Microbiology and Molecular Genetics, UMDNJ-New Jersey Medical School, Newark
[6] New Jersey Medical School, UMDNJ-New Jersey Medical School, Newark
[7] PPD, Washington, DC 20005
关键词
Human Immunodeficiency Virus; Peripheral Blood Mononuclear Cell; Blood Culture; Human Immunodeficiency Virus Infection; Human Immunodeficiency Virus Patient;
D O I
10.1186/1742-6405-3-5
中图分类号
学科分类号
摘要
Intracellular levels of glutathione are depleted in patients with acquired immunodeficiency syndrome in whom the risk of tuberculosis, particularly disseminated disease is many times that of healthy individuals. In this study, we examined the role of glutathione in immunity against tuberculosis infection in samples derived from healthy and human immunodeficiency virus infected subjects. Our studies confirm that glutathione levels are reduced in peripheral blood mononuclear cells and in red blood cells isolated from human immunodeficiency virus-infected subjects (CD4>400/cumm). Furthermore, treatment of blood cultures from human immunodeficiency virus infected subjects with N-acetyl cysteine, a glutathione precursor, caused improved control of intracellular M. tuberculosis infection. N-acetyl cysteine treatment decreased the levels of IL-1, TNF-α, and IL-6, and increased the levels of IFN-γ in blood cultures derived from human immunodeficiency virus-infected subjects, promoting the host immune responses to contain M. tuberculosis infection successfully. © 2006 Venketaraman et al; licensee BioMed Central Ltd.
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