Glutathione depletion is linked with Th2 polarization in mice with a retrovirus-induced immunodeficiency syndrome, murine AIDS: Role of proglutathione molecules as immunotherapeutics
Journal of Virology, ISSN: 1098-5514, Vol: 90, Issue: 16, Page: 7118-7130
2016
- 32Citations
- 30Captures
- 1Mentions
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations32
- Citation Indexes32
- 32
- CrossRef29
- Captures30
- Readers30
- 30
- Mentions1
- Blog Mentions1
- Blog1
Article Description
Injection of the LP-BM5 murine leukemia virus into mice causes murine AIDS, a disease characterized by many dysfunctions of immunocompetent cells. To establish whether the disease is characterized by glutathione imbalance, reduced glutathione (GSH) and cysteine were quantified in different organs. A marked redox imbalance, consisting of GSH and/or cysteine depletion, was found in the lymphoid organs, such as the spleen and lymph nodes. Moreover, a significant decrease in cysteine and GSH levels in the pancreas and brain, respectively, was measured at 5 weeks postinfection. The Th2 immune response was predominant at all times investigated, as revealed by the expression of Th1/Th2 cytokines. Furthermore, investigation of the activation status of peritoneal macrophages showed that the expression of genetic markers of alternative activation, namely, Fizz1, Ym1, and Arginase1, was induced. Conversely, expression of inducible nitric oxide synthase, a marker of classical activation of macrophages, was detected only when Th1 cytokines were expressed at high levels. In vitro studies revealed that during the very early phases of infection, GSH depletion and the downregulation of interleukin-12 (IL-12) p40 mRNA were correlated with the dose of LP-BM5 used to infect the macrophages. Treatment of LP-BM5-infected mice with N-(N-acetyl-L-cysteinyl)-S-acetylcysteamine (I-152), an N-acetyl-cysteine supplier, restored GSH/cysteine levels in the organs, reduced the expression of alternatively activated macrophage markers, and increased the level of gamma interferon production, while it decreased the levels of Th2 cytokines, such as IL-4 and IL-5. Our findings thus establish a link between GSH deficiency and Th1/Th2 disequilibrium in LP-BM5 infection and indicate that I-152 can be used to restore the GSH level and a balanced Th1/Th2 response in infected mice.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84982238873&origin=inward; http://dx.doi.org/10.1128/jvi.00603-16; http://www.ncbi.nlm.nih.gov/pubmed/27226373; https://journals.asm.org/doi/10.1128/JVI.00603-16; http://jvi.asm.org/lookup/doi/10.1128/JVI.00603-16; https://syndication.highwire.org/content/doi/10.1128/JVI.00603-16; https://digitalcommons.dartmouth.edu/facoa/1682; https://digitalcommons.dartmouth.edu/cgi/viewcontent.cgi?article=2685&context=facoa; https://dx.doi.org/10.1128/jvi.00603-16; https://journals.asm.org/doi/abs/10.1128/JVI.00603-16; https://jvi.asm.org/content/90/16/7118; https://jvi.asm.org/content/90/16/7118.abstract; https://jvi.asm.org/content/jvi/90/16/7118.full.pdf; http://jvi.asm.org/content/90/16/7118; https://jvi.asm.org/content/90/16/7118.full.pdf; http://jvi.asm.org/content/early/2016/05/19/JVI.00603-16; https://jvi.asm.org/content/early/2016/05/19/JVI.00603-16; https://jvi.asm.org/content/early/2016/05/19/JVI.00603-16.abstract; https://jvi.asm.org/content/early/2016/05/19/JVI.00603-16.full.pdf
American Society for Microbiology
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