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. 2025 Aug 20;17(8):1143.
doi: 10.3390/v17081143.

Cannabis Use Moderates Methamphetamine- and HIV-Related Inflammation: Evidence from Human Plasma Markers

Jeffrey M Rogers  1 , Victoria O Chentsova  1 , Crystal X Wang  2 , Maria Cecilia Garibaldi Marcondes  3 , Mariana Cherner  2 , Ronald J Ellis  2   4 , Scott L Letendre  2   5 , Robert K Heaton  2 , Igor Grant  2 , Jennifer E Iudicello  2
Affiliations

Cannabis Use Moderates Methamphetamine- and HIV-Related Inflammation: Evidence from Human Plasma Markers

Jeffrey M Rogers et al. Viruses. .

Abstract

Background: Methamphetamine use, which is disproportionately prevalent among people with HIV, increases risk for cardio- and neurovascular pathology through persistent immune activation and inflammation. Preclinical studies indicate that cannabinoids may reduce markers of pro-inflammatory processes, but data from people with chronic inflammatory conditions are limited. We examined potentially interacting associations of lifetime methamphetamine use disorder (MUD), recent cannabis use, and HIV with four plasma markers of immune and inflammatory functions.

Method: Participants with HIV (PWH, n = 86) and without HIV (PWoH, n = 148) provided urine and blood samples and completed neuromedical, psychiatric, and substance use assessments. Generalized linear models examined main and conditional associations of lifetime MUD, past-month cannabis use, and HIV with plasma concentrations of CXCL10/IP-10, CCL2/MCP-1, ICAM-1, and VCAM-1.

Results: PWH displayed higher CXCL10/IP-10 than PWoH. Past-month cannabis use was independently associated with lower CXCL10/IP-10 levels and conditionally lower CCL2/MCP-1, ICAM-1, and VCAM-1 levels among people with lifetime MUD, but only PWoH displayed cannabis-associated lower VCAM-1 levels.

Conclusions: Human plasma sample evidence suggests that cannabis use is associated with lower levels of immune and inflammatory molecules in the context of MUD or HIV. Cannabinoid pathways may be worthwhile clinical targets for treating sequelae of chronic inflammatory conditions.

Keywords: HIV; cannabinoids; central nervous system stimulant; inflammatory signaling pathways; methamphetamine; polysubstance use; substance use disorder.

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Conflict of interest statement

The authors declare no conflicts of interest and that funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Displayed are main associations of HIV status and past-month cannabis use with CXCL10/IP-10 levels, estimated from generalized linear regression models. PWH displayed significantly higher CXCL10/IP10 levels than PWoH (B = 0.54, p < .001), and those with past-month cannabis use displayed significantly lower levels (B = −0.33, p = .004).
Figure 2
Figure 2
Displayed are model-fitted distributions of CCL2/MCP-1 (top panel) and ICAM-1 (bottom panel), split by lifetime MUD (+/−) and recent cannabis use (C+/C−). Participants with MUD but not recent cannabis use (MUD+C−, blue) displayed significantly higher CCL2/MCP-1 (B = 0.36, p = .030) and ICAM-1 (B = 0.26, p = .007) levels than the comparison group (MUD−C−, yellow).
Figure 3
Figure 3
Displayed are model-fitted VCAM-1 distributions, split by lifetime MUD (+/−) and recent cannabis use (C+/C−), as well as HIV status (PWH in top panel, PWoH in bottom panel). Those with past-month cannabis use (MUD−C+, green) displayed lower VCAM-1 than the comparison group (MUD−C−, yellow) in PWH (top panel), but not in PWoH (bottom panel). Those with MUD but not recent cannabis use (MUD+C−, blue) displayed significantly higher VCAM-1 levels in PWoH (bottom panel), but not in PWH (top panel).
Figure 4
Figure 4
Displayed are model-fitted conditional associations between total lifetime days and grams of METH use, past-month cannabis use, and plasma levels of CCL2/MCP-1. Total METH days and total METH grams were only associated with CCL2/MCP1 in those with past-month cannabis use (C+, green).
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