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HIV-infected cannabis users have lower circulating CD16+ monocytes and IP-10 levels compared to non-using HIV patients

Rizzo Michael D.; Crawford, Robert B.; Henriquez, Joseph E.; Aldhamen, Yasser; Gulick, Peter; Amalfitano, Andrea; Kaminski, Norbert E.
doi: 10.1097/QAD.0000000000001704
ORIGINAL ARTICLE: PDF Only

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 interferon-γ-inducible protein 10 (IP-10) between HIV-infected cannabis users (HIV+MJ+) and non-cannabis users (HIV+MJ-), and determine whether in vitro 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 serum IP-10 from HIV+MJ- and HIV+MJ+ donors. Peripheral blood mononuclear cells (PBMC) 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 serum IP-10, compared to HIV+MJ- donors. Further, monocytes from HIV+MJ+ donors were unable to induce CD16 expression when treated with in vitro IFNα, while 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.

Conclusions:

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

Correspondence to Norbert E. Kaminski, Michigan State University, East Lansing, Michigan UNITED STATES. Tel: +517 353 3786; e-mail: kamins11@msu.edu

Received 28 August, 2017

Revised 20 October, 2017

Accepted 31 October, 2017

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Copyright © 2018 Wolters Kluwer Health, Inc.