HIV-infected cannabis users have lower circulating CD16+ monocytes and IFN-γ-inducible protein 10 levels compared with nonusing HIV patients

Components of cannabis, including THC, may decelerate peripheral monocyte processes that are implicated in HIV-associated neuroinflammation.

Flow cytometry was used to measure the number of blood CD16 monocytes and plasma IP-10 from HIV+MJ- and HIV+MJ+ donors. Peripheral blood mononuclear cells were isolated from HIV-MJ- and HIV+ (MJ- and MJ+) donors for in-vitro THC and IFNα treatment, and CD16 monocytes and supernatant IP-10 were quantified.

Chronic immune activation and elevated numbers of circulating activated monocytes (CD16) are implicated in HIV-associated neuroinflammation. The objective was to compare the level of circulating CD16 monocytes and IFN-γ-inducible protein 10 (IP-10) between HIV-infected cannabis users (HIV+MJ+) and noncannabis users (HIV+MJ-) and determine whether in-vitro Δ-Tetrahydrocannabinol (THC), a constituent of cannabis, affected CD16 expression as well as IP-10 production by monocytes. Design: The levels of circulating CD16 monocytes and IP-10 from HIV+MJ- and HIV+MJ+ donors were examined. In-vitro experimentation using THC was performed on primary leukocytes isolated from HIV-MJ-, HIV+MJ- and HIV+MJ+ donors to determine if THC has an impact on CD16 monocyte and IP-10 levels.

HIV+MJ+ donors possessed a lower level of circulating CD16 monocytes and plasma IP-10, compared with HIV+MJ- donors. Further, monocytes from HIV+MJ+ donors were unable to induce CD16 expression when treated with in-vitro IFNα, whereas HIV-MJ- and HIV+MJ- donors displayed pronounced CD16 induction, suggesting anti-inflammatory effects by cannabis. Lastly, in-vitro THC treatment impaired CD16 monocyte transition to CD16 and monocyte-derived IP-10.