ArticleJournal of neuroinflammation2017
Contrasting effect of the latency-reversing agents bryostatin-1 and JQ1 on astrocyte-mediated neuroinflammation and brain neutrophil invasion.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Neutrophils-astrocyte interactions in central nervous system inflammation.Cell death & disease · 2025Review
- A 3D In Vitro Blood-Brain Barrier Model to Study Pathogen and Drug Effects on the BBB.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Virus-Shaped Mesoporous Silica Nanostars to Improve the Transport of Drugs across the Blood-Brain Barrier.ACS applied materials & interfaces · 2024Article
- Differential effects of SARS-CoV-2 variants on central nervous system cells and blood-brain barrier functions.Journal of neuroinflammation · 2023Article
- HIV infection of non-classical cells in the brain.Retrovirology · 2023Review
- Shock and kill within the CNS: A promising HIV eradication approach?Journal of leukocyte biology · 2022Review
- Nanostars Carrying Multifunctional Neurotrophic Dendrimers Protect Neurons in Preclinical In Vitro Models of Neurodegenerative Disorders.ACS applied materials & interfaces · 2022Article
- HIV Latency in Myeloid Cells: Challenges for a Cure.Pathogens (Basel, Switzerland) · 2022Review
- Altered expression of fractalkine in HIV-1-infected astrocytes and consequences for the virus-related neurotoxicity.Journal of neurovirology · 2021Article
- Network-Based Analysis of OMICs Data to Understand the HIV-Host Interaction.Frontiers in microbiology · 2020Review
- HIV Eradication Strategies: Implications for the Central Nervous System.Current HIV/AIDS reports · 2019Review
- Antiretroviral drug-S for a possible HIV elimination.International journal of physiology, pathophysiology and pharmacology · 2019Article
- (+)-JQ1 attenuated LPS-induced microglial inflammation via MAPK/NFκB signaling.Cell & bioscience · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDespite effectiveness of the combined antiretroviral therapy, HIV-1 persists in long-lived latently infected cells. Consequently, new therapeutic approaches aimed at eliminating this latent reservoir are currently being developed. A "shock and kill" strategy using latency-reversing agents (LRA) to reactivate HIV-1 has been proposed. However, the impact of LRA on the central nervous system (CNS) remains elusive.
methodsWe used human fetal astrocytes and investigated the effects of several LRA on their functional and secretory activities. Astrocytes were infected with VSV-G-pseudotyped HIV-1 before treatment with various blood-brain barrier (BBB)-permeable LRA at subcytotoxic doses, which allow HIV-1 reactivation based on previous in vitro and clinical studies. Cells and supernatants were then used to evaluate effects of infection and LRA on (i) viability and metabolic activity of astrocytes using a colorimetric MTS assay; (ii) chemokines and proinflammatory cytokines secretion and gene expression by astrocytes using ELISA and RT-qPCR, respectively; (iii) expression of complement component 3 (C3), a proxy for astrogliosis, by RT-qPCR; (iv) glutamate uptake capacity by a fluorometric assay; and (v) modulation of neutrophil transmigration across an in vitro BBB model.
resultsWe demonstrate that bryostatin-1 induces secretion of chemokines CCL2 and IL-8 and proinflammatory cytokines IL-6 and GM-CSF, whereas their production is repressed by JQ1. Bryostatin-1 also increases expression of complement component 3 and perturbs astrocyte glutamate homeostasis. Lastly, bryostatin-1 enhances transmigration of neutrophils across an in vitro blood-brain barrier model and induces formation of neutrophil extracellular traps.
conclusionsThese observations highlight the need to carefully assess the potential harmful effect to the CNS when selecting LRA for HIV-1 reactivation strategies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.