Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection
We examined the causes for decreased glutathione (GSH) in individuals with HIV infection. We observed lower levels of intracellular GSH in macrophages from individuals with HIV compared to healthy subjects. Further, the GSH composition found in macrophages from HIV+ subjects heavily favors oxidized...
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Format: | Article |
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Wiley
2012-01-01
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Series: | Clinical and Developmental Immunology |
Online Access: | http://dx.doi.org/10.1155/2012/734125 |
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author | Devin Morris Carlos Guerra Clare Donohue Hyoung Oh Melissa Khurasany Vishwanath Venketaraman |
author_facet | Devin Morris Carlos Guerra Clare Donohue Hyoung Oh Melissa Khurasany Vishwanath Venketaraman |
author_sort | Devin Morris |
collection | DOAJ |
description | We examined the causes for decreased glutathione (GSH) in individuals with HIV infection. We observed lower levels of intracellular GSH in macrophages from individuals with HIV compared to healthy subjects. Further, the GSH composition found in macrophages from HIV+ subjects heavily favors oxidized glutathione (GSSG) which lacks antioxidant activity, over free GSH which is responsible for GSH’s antioxidant activity. This decrease correlated with an increase in the growth of Mycobacterium tuberculosis (M. tb) in macrophages from HIV+ individuals. In addition, we observed increased levels of free radicals, interleukin-1 (IL-1), interleukin-17 (IL-17) and transforming growth factor-β (TGF-β) in plasma samples derived from HIV+ individuals compared to healthy subjects. We observed decreased expression of the genes coding for enzymes responsible for de novo synthesis of GSH in macrophages derived from HIV+ subjects using quantitative PCR (qPCR). Our results indicate that overproduction of proinflammatory cytokines in HIV+ individuals lead to increased production of free radicals. This combined with the decreased expression of GSH synthesis enzymes leads to a depletion of free GSH and may lead in part to the loss of immune function observed in HIV patients. |
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id | doaj-art-6c22b3910b4b4885b458351b9cd095ad |
institution | Kabale University |
issn | 1740-2522 1740-2530 |
language | English |
publishDate | 2012-01-01 |
publisher | Wiley |
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series | Clinical and Developmental Immunology |
spelling | doaj-art-6c22b3910b4b4885b458351b9cd095ad2025-02-03T06:00:17ZengWileyClinical and Developmental Immunology1740-25221740-25302012-01-01201210.1155/2012/734125734125Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV InfectionDevin Morris0Carlos Guerra1Clare Donohue2Hyoung Oh3Melissa Khurasany4Vishwanath Venketaraman5Graduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, CA 91766, USAScience Department, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766, USAPitzer College, 1050 N Mills Avenue, Claremont, CA 91711, USAGraduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, CA 91766, USACollege of Dental Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766, USAGraduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, CA 91766, USAWe examined the causes for decreased glutathione (GSH) in individuals with HIV infection. We observed lower levels of intracellular GSH in macrophages from individuals with HIV compared to healthy subjects. Further, the GSH composition found in macrophages from HIV+ subjects heavily favors oxidized glutathione (GSSG) which lacks antioxidant activity, over free GSH which is responsible for GSH’s antioxidant activity. This decrease correlated with an increase in the growth of Mycobacterium tuberculosis (M. tb) in macrophages from HIV+ individuals. In addition, we observed increased levels of free radicals, interleukin-1 (IL-1), interleukin-17 (IL-17) and transforming growth factor-β (TGF-β) in plasma samples derived from HIV+ individuals compared to healthy subjects. We observed decreased expression of the genes coding for enzymes responsible for de novo synthesis of GSH in macrophages derived from HIV+ subjects using quantitative PCR (qPCR). Our results indicate that overproduction of proinflammatory cytokines in HIV+ individuals lead to increased production of free radicals. This combined with the decreased expression of GSH synthesis enzymes leads to a depletion of free GSH and may lead in part to the loss of immune function observed in HIV patients.http://dx.doi.org/10.1155/2012/734125 |
spellingShingle | Devin Morris Carlos Guerra Clare Donohue Hyoung Oh Melissa Khurasany Vishwanath Venketaraman Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection Clinical and Developmental Immunology |
title | Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection |
title_full | Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection |
title_fullStr | Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection |
title_full_unstemmed | Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection |
title_short | Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection |
title_sort | unveiling the mechanisms for decreased glutathione in individuals with hiv infection |
url | http://dx.doi.org/10.1155/2012/734125 |
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