Cooperative induction of CXCL10 involves NADPH oxidase: Implications for HIV dementia.

Glia
Rachel WilliamsShilpa Buch

Abstract

With the increasing prevalence of HIV-associated neurocognititve disorders (HAND), understanding the mechanisms by which HIV-1 induces neuro-inflammation and subsequent neuronal damage is important. The hallmark features of HIV-encephalitis, the pathological correlate of HIV-associated Dementia (HAD), are gliosis, oxidative stress, chemokine dysregulation, and neuronal damage/death. Since neurons are not infected by HIV-1, the current thinking is that these cells are damaged indirectly by pro-inflammatory chemokines released by activated glial cells. CXCL10 is a neurotoxic chemokine that is upregulated in astroglia activated by HIV-1 Tat, IFN-gamma, and TNF-alpha. In this study we have demonstrated that HIV-1 Tat increases CXCL10 expression in IFN-gamma and TNF-alpha stimulated human astrocytes via NADPH oxidase. We have shown that the treatment of astrocytes with a mixture of Tat and cytokines leads to a respiratory burst that is abrogated by apocynin, an NADPH oxidase inhibitor. Pretreatment of Tat, IFN-gamma, and TNF-alpha stimulated astrocytes with apocynin also resulted in concomitant inhibition of CXCL10 expression. Additionally, apocynin was also able to reduce Tat and cytokine-mediated activation of the corresponding si...Continue Reading

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Citations

Apr 1, 2010·Journal of Neuroimmune Pharmacology : the Official Journal of the Society on NeuroImmune Pharmacology·Honghong YaoShilpa J Buch
Feb 26, 2010·Journal of Virology·Alan C JacksonPaul Fernyhough
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Nov 12, 2015·Frontiers in Microbiology·Sonia MediouniSusana T Valente
Nov 17, 2020·Frontiers in Microbiology·Javier UrquizaJorge Quarleri
Aug 25, 2021·Current HIV/AIDS Reports·Susmita SilShilpa Buch

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