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Cited by 12Neuroinflammation and Neurodegeneration MechanismsInflammasome and immune disordersAutophagy in Disease and Therapy

Role of Dysregulated Autophagy in HIV Tat, Cocaine, and cART Mediated NLRP3 Activation in Microglia

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Singh, Seema, Thangaraj, Annadurai, Chivero, Ernest T., Guo, Ming-Lei, Periyasamy, Palsamy, Buch, Shilpa·2023·Journal of Neuroimmune Pharmacology
DOI 10.1007/s11481-023-10063-0PMC PMC10729649
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Abstract

Despite the ability of combination antiretroviral therapy (cART) to suppress viremia, there is persistence low levels of HIV proteins such as Transactivator of transcription (Tat) in the central nervous system (CNS), contributing to glial activation and neuroinflammation. Accumulating evidence also implicates the role of drugs of abuse in exacerbating neurological complications associated with HIV-1. The combined effects of HIV Tat, drugs of abuse, and cART can thus create a toxic milieu in the CNS. The present study investigated the combinatorial effects of HIV-Tat, cocaine, and cART on autophagy and NLRP3 inflammasome activation. We selected a combination of three commonly used cART regimens: tenofovir, emtricitabine, and dolutegravir. Our results demonstrated that exposure of mouse primary microglia (MPMs) to these agents-HIV Tat (25 ng/ml), cocaine (1 μM), and cART (1 μM each) resulted in upregulation of autophagy markers: Beclin1, LC3B-II, and SQSTM1 with impaired lysosomal functioning involving increased lysosomal pH, decreased LAMP2 and cathepsin D, ultimately leading to dysregulated autophagy. Our findings also demonstrated activation of the NLRP3 signaling in microglia exposed to these agents. We further demonstrated that gene silencing of key autophagy protein BECN1 significantly blocked NLRP3-mediated activation of microglia. Silencing of NLRP3, however, failed to block HIV Tat, cocaine, and cART-mediated dysregulation of the autophagy-lysosomal axis; these in vitro phenomena were also validated in vivo using iTat mice administered cocaine and cART. This study thus underscores the cooperative effects of HIV Tat, cocaine, and cART in exacerbating microglial activation involving dysregulated autophagy and activation of the NLRP3 inflammasome signaling.

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  • HIV-TAT can damage lysosome function in microglia and in neuron.

    “HIV-TAT can damage lysosome function in microglia and in neuron [46, 75].”

    From HIV-TAT dysregulates microglial lipid metabolism through SREBP2/miR-124 axis: Implication of lipid droplet accumulation microglia in NeuroHIV (2025) · cites this paper as [46]

    The Results section, “HIV Tat, Cocaine, and cART Co-operatively Impair the Lysosomal Function in MPMs” (page not provided), reports impaired lysosomal function in mouse primary microglia exposed to the three agents together. It does not establish that Tat alone damages lysosomes, and it does not report lysosomal damage in neurons. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

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Sorted by citations

Authors
Singh, S., Thangaraj, A., Chivero, E. T., Guo, M.-L., Periyasamy, P., & Buch, S.
Affiliations
  • Nebraska Medical Center (US)
  • University of Nebraska at Omaha (US)
  • Eastern Virginia Medical School (US)
  • University of Nebraska Medical Center (US)
Corresponding author
  • Guo, Ming-Lei
  • Periyasamy, Palsamy
  • Buch, Shilpa
ORCID
Venue
Journal of Neuroimmune Pharmacology
Publisher
Springer Science and Business Media LLC
Published
2023-05-06
Volume
18
Issue
3
Pages
327-347
ISSN
  • 1557-1890 (ISSN-L)
  • 1557-1904
DOI
10.1007/s11481-023-10063-0
PMC
PMC10729649
OpenAlex
W4372352752
Cited by
12
References
1
Citations by year
2026: 3 · 2025: 3 · 2024: 5 · 2023: 1
FWCI
1.24
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Neuroimmune Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Drug Abuse (R01DA047156, R01DA050545)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
HIV-1 Tat protein, cocaine, highly active antiretroviral therapy, NLRP3 inflammasome, microglia, autophagy dysregulation, neuroinflammation, tenofovir, emtricitabine, dolutegravir, Beclin-1, lysosomal dysfunction, HIV-associated neurocognitive disorders
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Autophagy, Cocaine, Trans-Activators, HIV Infections, Microglia, Mice, tat Gene Products, Human Immunodeficiency Virus, Inflammasomes

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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