Dr. Weeks’ Comment: Mycobacterium is like a cross between the worst bacteria and the worst fungus: it is hard to kill. Phage therapy is the best option but if it is avian (in the lungs) remember to use nebulized glutathione.
AIDS Res Ther. 2006 Feb 20;3:5.
Glutathione and growth inhibition of Mycobacterium tuberculosis in healthy and HIV infected subjects.
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-alpha, and IL-6, and increased the levels of IFN-gamma in blood cultures derived from human immunodeficiency virus-infected subjects, promoting the host immune responses to contain M. tuberculosis infection successfully.
Microb Pathog. 2008 Mar;44(3):255-61. Epub 2007 Sep 26.
Glutathione levels and immune responses in tuberculosis patients.
1Division of Infectious Diseases, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA. firstname.lastname@example.org
Glutathione levels are significantly reduced in peripheral blood mononuclear cells and red blood cells isolated from tuberculosis patients. Treatment of blood cultures from tuberculosis patients with N-acetyl cysteine, a glutathione precursor, was associated with improved control of intracellular M. tuberculosis infection. N-acetyl-cysteine treatment decreased the levels of IL-10, IL-6, TNF-alpha and IL-1, in blood cultures derived from tuberculosis patients, favoring the host immune cells to successfully control M. tuberculosis replication.