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Cannabinoids inhibit migration of microglial-like cells to the HIV protein Tat

Daniel Fraga1, Erinn S Raborn, Gabriela A Ferreira

  • 1Department of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, 1101 E. Marshall St., Richmond, VA 23298, USA.

Journal of Neuroimmune Pharmacology : the Official Journal of the Society on Neuroimmune Pharmacology
|July 8, 2011
PubMed

Insights

Cannabinoids like THC reduce microglial cell migration towards HIV Tat protein by activating the CB2 receptor. This suggests cannabinoids may help manage HIV-related neuroinflammation by controlling microglial movement.

Area of Science:

  • Neuroimmunology
  • Pharmacology
  • Virology

Background:

  • Microglia, the immune cells of the central nervous system (CNS), release inflammatory factors, including HIV Tat protein, contributing to HIV neuropathogenesis.
  • HIV Tat protein stimulates microglial migration via beta-chemokine receptors, exacerbating neuroinflammation.
  • Cannabinoids possess anti-inflammatory properties and can cross the blood-brain barrier, offering potential therapeutic avenues for neuroimmune disorders.

Purpose of the Study:

  • To investigate the effects of specific cannabinoids on microglial cell migration induced by HIV Tat protein.
  • To determine the role of cannabinoid receptors, specifically CB1R and CB2R, in mediating these effects.

Main Methods:

  • Utilized a mouse BV-2 microglial cell model to assess migration towards Tat.
  • Administered exogenous cannabinoids (Delta-9-tetrahydrocannabinol [THC], CP55940) and an endogenous cannabinoid (2-arachidonoylglycerol [2-AG]).
  • Employed CB1R and CB2R antagonists (SR141716A, SR144528) and CB2R knockdown via small interfering RNA (siRNA) to elucidate receptor involvement.
  • Analyzed changes in the beta-chemokine receptor CCR-3 expression and localization.

Main Results:

  • Exogenous and endogenous cannabinoids significantly reduced BV-2 cell migration towards Tat in a concentration-dependent manner.
  • The inhibitory effect was blocked by the CB2R antagonist SR144528 but not by the CB1R antagonist SR141716A.
  • CB2R knockdown reversed the cannabinoid-mediated inhibition of migration.
  • Cannabinoid treatment altered the expression and intracellular compartmentation of the beta-chemokine receptor CCR-3.

Conclusions:

  • Cannabinoid-mediated inhibition of microglial migration to HIV Tat is functionally linked to the CB2 receptor.
  • Activation of CB2R by cannabinoids modulates the expression and localization of CCR-3, impacting microglial response to Tat.
  • These findings highlight the therapeutic potential of CB2R-targeting cannabinoids in managing HIV-associated neuroinflammation.

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