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HIV-infected cannabis users have lower circulating CD16+ monocytes and IFN-γ-inducible protein 10 levels compared
Michael D Rizzo1,2, Robert B Crawford2,3, Joseph E Henriquez2,3
1Cell & Molecular Biology Program.
Insights
Cannabis use in HIV patients may reduce neuroinflammation markers like CD16 monocytes and IP-10. Delta-Tetrahydrocannabinol (THC) in cannabis appears to dampen monocyte activation and inflammatory responses.
Area of Science:
- Neuroimmunology
- Pharmacology
Background:
- Chronic immune activation and elevated CD16 monocytes are linked to HIV-associated neuroinflammation.
- IFN-γ-inducible protein 10 (IP-10) is a key inflammatory marker in HIV.
Purpose of the Study:
- To compare CD16 monocyte and IP-10 levels in HIV-infected cannabis users (HIV+MJ+) versus non-users (HIV+MJ-).
- To investigate the in-vitro effects of Δ-Tetrahydrocannabinol (THC) on CD16 expression and IP-10 production by monocytes.
Main Methods:
- Flow cytometry was used to quantify circulating CD16 monocytes and plasma IP-10.
- Primary leukocytes from HIV-negative, HIV+MJ-, and HIV+MJ+ donors were treated in-vitro with THC and IFNα.
Main Results:
- HIV+MJ+ donors showed lower circulating CD16 monocytes and plasma IP-10 compared to HIV+MJ- donors.
- Monocytes from HIV+MJ+ donors exhibited reduced CD16 induction by IFNα, suggesting anti-inflammatory properties.
- In-vitro THC impaired CD16 monocyte transition and monocyte-derived IP-10 production.
Conclusions:
- Cannabis components, including THC, may mitigate monocyte-driven processes contributing to HIV-associated neuroinflammation.
- THC demonstrates potential anti-inflammatory effects on monocytes relevant to HIV pathogenesis.
Objective:
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.
Methods:
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.
Results:
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.
Conclusion:
Components of cannabis, including THC, may decelerate peripheral monocyte processes that are implicated in HIV-associated neuroinflammation.
