ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Buprenorphine decreases the CCL2-mediated chemotactic response of monocytes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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Who cites it
27 citing papers in PubMed, 33 citations in OpenAlex.
- Preliminary evidence of neuroimmune system disruption in opioid use disorder: Findings from a pilot PET TSPO imaging study.Brain, behavior, & immunity - health · 2026Article
- Review
- Buprenorphine extended-release (Ethiqa XR) impacts the immunological response in mice exposed to aerosolizedFrontiers in immunology · 2026Article
- Buprenorphine's Effect on the Human Immune System and Inflammation.Clinical and translational science · 2025Review
- Role of Monocyte/Macrophages in the Pathogenesis of NeuroHIV.Results and problems in cell differentiation · 2024Review
- Monocyte depletion enhances neutrophil influx and proneural to mesenchymal transition in glioblastoma.Nature communications · 2023Article
- Sex-Specific Effects of Buprenorphine on Endoplasmic Reticulum Stress, Abnormal Protein Accumulation, and Cell Loss After Pediatric Mild Traumatic Brain Injury in Mice.Neurotrauma reports · 2023Article
- Disruption of monocyte-macrophage differentiation and trafficking by a heme analog during active inflammation.Mucosal immunology · 2022Article
- Single-cell analysis reveals chemokine-mediated differential regulation of monocyte mechanics.iScience · 2022Article
- Buprenorphine reverses neurocognitive impairment in EcoHIV infected mice: A potential therapy for HIV-NCI.Frontiers in immunology · 2022Article
- The Roles of Junctional Adhesion Molecules (JAMs) in Cell Migration.Frontiers in cell and developmental biology · 2022Review
- Buprenorphine Increases HIV-1 Infection In Vitro but Does Not Reactivate HIV-1 from Latency.Viruses · 2021Article
- Treatment with buprenorphine prior to EcoHIV infection of mice prevents the development of neurocognitive impairment.Journal of leukocyte biology · 2021Article
- Design and implementation of a prospective cohort study of persons living with and without HIV infection who are initiating medication treatment for opioid use disorder.Contemporary clinical trials communications · 2021Article
- Opioid and neuroHIV Comorbidity - Current and Future Perspectives.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
- Naringin provides neuroprotection in CCL2-induced cognition impairment by attenuating neuronal apoptosis in the hippocampus.Behavioral and brain functions : BBF · 2020Article
- Tanshinone IIA Alleviates CCL2-Induced Leaning memory and Cognition Impairment in Rats: A Potential Therapeutic Approach for HIV-Associated Neurocognitive Disorder.BioMed research international · 2020Article
- The impact of substance abuse on HIV-mediated neuropathogenesis in the current ART era.Brain research · 2019Review
- Do All Opioid Drugs Share the Same Immunomodulatory Properties? A Review From Animal and Human Studies.Frontiers in immunology · 2019Review
- The Effects of Opioids on HIV Neuropathogenesis.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Despite successful combined antiretroviral therapy, ∼ 60% of HIV-infected people exhibit HIV-associated neurocognitive disorders (HAND). CCL2 is elevated in the CNS of infected people with HAND and mediates monocyte influx into the CNS, which is critical in neuroAIDS. Many HIV-infected opiate abusers have increased neuroinflammation that may augment HAND. Buprenorphine is used to treat opiate addiction. However, there are few studies that examine its impact on HIV neuropathogenesis. We show that buprenorphine reduces the chemotactic phenotype of monocytes. Buprenorphine decreases the formation of membrane projections in response to CCL2. It also decreases CCL2-induced chemotaxis and mediates a delay in reinsertion of the CCL2 receptor, CCR2, into the cell membrane after CCL2-mediated receptor internalization, suggesting a mechanism of action of buprenorphine. Signaling pathways in CCL2-induced migration include increased phosphorylation of p38 MAPK and of the junctional protein JAM-A. We show that buprenorphine decreases these phosphorylations in CCL2-treated monocytes. Using DAMGO, CTAP, and Nor-BNI, we demonstrate that the effect of buprenorphine on CCL2 signaling is opioid receptor mediated. To identify additional potential mechanisms by which buprenorphine inhibits CCL2-induced monocyte migration, we performed proteomic analyses to characterize additional proteins in monocytes whose phosphorylation after CCL2 treatment was inhibited by buprenorphine. Leukosialin and S100A9 were identified and had not been shown previously to be involved in monocyte migration. We propose that buprenorphine limits CCL2-mediated monocyte transmigration into the CNS, thereby reducing neuroinflammation characteristic of HAND. Our findings underscore the use of buprenorphine as a therapeutic for neuroinflammation as well as for addiction.
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Registered trials
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.