Researchers from Michigan State University report that THC and CBD may help reduce certain inflammatory processes tied to HIV-associated neurocognitive disorders, according to a new study published by the Journal of Neuroimmune Pharmacology.
The study focused on CD16+ monocytes, a small subset of immune cells that researchers say play an outsized role in neuroinflammation linked to HIV-associated neurocognitive disorders, also known as HAND. These cells are more likely than CD16- monocytes to migrate into the brain, where they can interact with brain-resident cells such as astrocytes and contribute to inflammation.
Despite cannabis use being common among people with HIV, researchers said the mechanisms by which cannabinoids influence immune responses related to HAND remain unclear. The study examined whether delta-9 THC and cannabidiol could suppress inflammatory signaling between CD16+ monocytes and astrocytes in the context of HIV-related immune activation.
Researchers found that both THC and CBD reduced CD16+ monocyte-driven astrocyte production of several inflammatory mediators, including IL-6, IL-8 and MCP-1, when the cells were exposed to stimulation of toll-like receptors 7 or 8. These receptors can be activated by HIV single-stranded RNA and are involved in immune responses that may contribute to neuroinflammation.
The study also found that monocytes from HIV-positive subjects showed increased migration compared to monocytes from HIV-negative subjects. THC treatment suppressed that enhanced migration, while CBD did not show the same effect. Researchers linked the THC-related reduction in migration to decreased expression of polymerized actin and high-affinity integrin receptors, both of which are involved in immune cell movement.
The findings suggest that THC, and to a lesser extent CBD, may have therapeutic potential for reducing CD16+ monocyte-mediated neuroinflammation associated with HIV-related neurocognitive disorders.
However, the study does not show that cannabis use treats or prevents HAND in patients. Instead, the findings point to possible biological mechanisms by which specific cannabinoids could influence immune activity related to HIV-associated neuroinflammation, warranting further research.
