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

Rizzo, Michael, D.a,b; Crawford, Robert, B.b,c; Henriquez, Joseph, E.b,c; Aldhamen, Yasser, A.d; Gulick, Petere; Amalfitano, Andread,e; Kaminski, Norbert, E.b,c

doi: 10.1097/QAD.0000000000001704
Basic Science

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 9-Tetrahydrocannabinol">Δ9-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.

aCell & Molecular Biology Program

bInstitute for Integrative Toxicology

cDepartment of Pharmacology & Toxicology

dDepartment of Microbiology & Molecular Genetics

eDepartment of Osteopathic Medicine, Michigan State University, East Lansing, Michigan, USA.

Correspondence to Norbert E. Kaminski, Department of Pharmacology & Toxicology, Michigan State University, East Lansing, Michigan, USA. Tel: +1 517 353 3786; e-mail: kamins11@msu.edu

Received 28 August, 2017

Revised 20 October, 2017

Accepted 31 October, 2017

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