RCMI-CCRHD Faculty Development Program 2023-2024 “Innate Immunity Responses in Monocytes: Contribution to Neurodegeneration”

Research Areas

  • Neuroinflammation & Neurodegeneration
  • Infectious Diseases
  • Viral Immunology

Scientific Achievements

  • Studied how innate immune responses and peripheral macrophages in HIV-associated neuronal injury and cognitive decline
  • Developed a brain organoid-macrophage co-culture model to understand how immune cells trigger neuroinflammation and neurodegeneration
  • Yamil Gerena, PhD & Valerie Wojna, MD, FAAN: Collazo, B.J., Ortiz-Valentín, L., Negrón-Rodríguez, C.G., Medina-Colón, J.C., Cantres-Rosario, Y.M., Rodriguez, E., Wojna, V. & Gerena, Y. Influence of plasma exosomes from women living with HIV Stratified by HAND on monocyte subpopulations from healthy women without HIV. J. Neurovirol. 31, 95–107 (2025).

Funding

RCMI Funding:

  • NIH/NIMHD U54MD007600

Other funding obtained with RCMI support:

  • K22NS118975 “Innate Immunity Responses In Monocytes: Contribution To Neurodegeneration”
  • UPR-MSC Title V Program #PO31S200104 Pilot Project: “Interplay between oral microbiome, the immune system, and neuronal function.”

Scientific Advance

Quantitative Proteomics Reveal That CB2R Agonist JWH-133 Downregulates NF-κB Activation, Oxidative Stress, and Lysosomal Exocytosis from HIV-Infected Macrophages
Published in International Journal of Molecular Sciences, Volume 25, 2024, PMCID: PMC10970132.
In this study, researchers treated macrophages infected by HIV with a compound called JWH-133 (an agonist of the cannabinoid receptor type 2, CB2R) and used a technique called quantitative proteomics to see how protein expression changes. They found that JWH-133 reduced activity of NF-κB (a protein complex that drives inflammation), lowered levels of oxidative stress, and decreased the release of lysosomal contents (which can contribute to cell damage) from the infected macrophages. These findings suggest that activating CB2R could help reduce inflammation and cellular damage in HIV-infected macrophages, potentially pointing toward a therapeutic strategy to protect immune cells in people living with HIV.
U54 MD007600/NIMHD NIH HHS/United States, P20 GM103475/NIGMS NIH HHS/United States, U54 GM133807/NIGMS NIH HHS/United States, R25 GM061838/NIGMS NIH HHS/United States, F99 NS113455/NINDS NIH HHS/United States
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