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

Vishwanath Venketaraman1,2,3,4,5,6 email, Tatanisha Rodgers1,4,6 email, Rafael Linares6 email, Nancy Reilly1,4,6 email, Shobha Swaminathan1,4,6 email, David Hom2,6 email, Ariel C Millman1,4,6 email, Robert Wallis1,4,6,7 email and Nancy D Connell1,2,3,4,5,6 email

Division of Infectious Diseases, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA

Center for Emerging and Re-emerging Pathogens, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA

National Tuberculosis Center, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA

Department of Medicine, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA

Department of Microbiology and Molecular Genetics, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA

New Jersey Medical School, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA

PPD, 1213 N Street NW, Apt. A, Washington DC 20005, USA

author email corresponding author email

AIDS Research and Therapy 2006, 3:5doi:10.1186/1742-6405-3-5

Published: 20 February 2006

Abstract

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.


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