Findings suggest cannabinoids may have an immunological benefit, limiting the risk of development of non-AIDS-associated comorbidities.
A recent study found that cannabis use is associated with a potentially beneficial reduction in systemic inflammation and immune activation in the context of antiretroviral therapy (ART)-treated HIV-infected individuals.
Findings concluded that heavy cannabis use, as defined by plasma quantity of THC-COOH, was associated with decreased frequencies of activated T cells and inflammatory antigen-presenting cell subsets, which suggests a potential immunologic benefit of cannabinoids through decreased immune activation in HIV-infected individuals.
“The novel finding is important given that elevated levels of T-cell activation have been associated with lower CD4+ T-cell gains following ART and with mortality in this population,” study authors wrote. “Thus, our work suggests that cannabinoids may have an immunological benefit in the context of HIV infection, as lowering the frequency of activated T cells could limit the risk of development of non-AIDS-associated comorbidities.”
Study authors sought to determine the impact of cannabis use on indicators of inflammation and immune activation in HIV-infected, ART-treated individuals, hypothesizing that regular cannabis use would be associated with decreased frequencies of inflammatory cells and a lowered expression of markers of immune activation and dysfunction.
“Medical cannabis use continues to expand, despite the ongoing restrictions on research that would enable physicians to properly counsel their patients on when and how it should be used,” David L. Nathan, MD, DFAPA, president of the board of directors, Doctors for Cannabis Regulation, told MD Magazine.
Researchers studied the impact of cannabis use on peripheral immune cell frequency, activation and function in 198 HIV-infected, ART-treated individuals by flow cytometry. Cryopreserved peripheral blood mono-nuclear cells and plasma samples were obtained from each participant.
Study participants were divided into 4 categories: heavy, medium or occasional cannabis users or non-cannabis users based on the amount of cannabis metabolite 11-nor-carboxy-tetrahydrocannabinol detected in plasma by mass spectrometry.
Sixty-five subjects self-identified as daily cannabis users, while 133 participants self-identified as never using cannabis.
Even though researchers concluded that the clinical implications of cannabis are unclear, heavy cannabis users were found to have decreased frequencies of intermediate and nonclassical monocyte subsets, as well as decreased frequencies of interleukin 23- and tumor necrosis factor alpha (TNF-α) producing antigen presenting cells compared to frequencies of activated T cells in non-cannabis-using individuals.
The results are consistent with previous studies demonstrating that cannabinoids can reduce immune cell cytokine production and cellular proliferation.
It’s also important to note, that in the study, researchers found that the moderate and heavy cannabis-using individuals had a significantly higher frequency of HCV-coinfected individuals compared to non-cannabis-using individuals. Despite the higher frequency of HCV coinfection, the individuals still have significantly lower indicators of inflammation and immune activation compared to non-cannabis-using groups.
Further studies are needed to clarify the exact effect that HCV and other common coinfections may have in the cannabis-using, HIV-infected population, as well as determine the mechanism that cannabis causes reduced immune activation.
“These findings have clinical implications, as cannabinoids may have an immunological benefit and nonpsychoactive cannabis derivatives could be investigated as novel therapeutics to be used in conjunction with ART to aid in reduction of persistent inflammation,” study authors concluded.
The study, "Heavy Cannabis Use Associated With Reduction in Activated and Inflammatory Immune Cell Frequencies in Antiretroviral Therapy—Treated Human Immunodeficiency Virus-Infected Individuals" was published February 2018 in the Clinical Infectious Disease.