# Cannabidiol and Macrophage Chronic Inflammation in a Virally Suppressed Rhesus Macaque Model

> **NIH NIH R01** · JOHNS HOPKINS UNIVERSITY · 2021 · $162,676

## Abstract

PROJECT SUMMARY/ABSTRACT
Chronic, immune activation is one of the major hallmarks of HIV in the modern era, despite the effectiveness of
antiretroviral therapy (ART) in suppressing viral replication. This chronic immune activation is largely mediated
by myeloid-lineage cells, including monocytes, macrophages, and microglia. This demonstrates a critical need
to develop new anti-inflammatory strategies that are effective in inhibiting myeloid activation in the context of
chronic HIV infection and treatment. Cannabinoids, particularly the phytocannabinoid cannabidiol (CBD) is
among the most promising new anti-inflammatory drug. However, the impact of CBD on HIV/SIV associated
inflammation is not clear because there have been no studies assessing the anti-inflammatory properties of
cannabidiol (CBD) in the SIV/macaque model of HIV. There is a pressing need to better counteract HIV-
associated inflammation in the ART era. Given the gap in our knowledge regarding the immunomodulatory
effects of cannabinoids, we propose studies on CBD administration in a virally suppressed rhesus macaque
model (ART-SIV). Resident tissue macrophages express functional CB1, CB2, and GPR55, though there is
variable expression among the organs. Our data show that stimulating these receptors inhibits endogenous
and LPS-induced pro-inflammatory and anti-viral genes, while increasing potent anti-inflammatory cytokines.
We determined that these cytokines were a source of chronic inflammation in the periphery and CNS in our
SIV-ART model. Thus, we propose to 1) evaluate the impact of CBD on myeloid immune activation, 2)
determine the effect of CBD on myeloid antiviral signatures, and 3) define the impact of CBD on the monocytic
and microglial neuroinflammatory and neuroprotective transcriptome. We anticipate our work will provide
insight into the mechanisms by which CBD exerts anti-inflammatory properties, both peripherally and in the
brain. Additionally, our findings will fill a critical gap in knowledge regarding the inflammatory mechanisms
underlying CNS dysfunction in the current ART era.

## Key facts

- **NIH application ID:** 10455888
- **Project number:** 3R01DA052859-02S1
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Dionna Whitney Williams
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $162,676
- **Award type:** 3
- **Project period:** 2020-09-30 → 2025-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10455888

## Citation

> US National Institutes of Health, RePORTER application 10455888, Cannabidiol and Macrophage Chronic Inflammation in a Virally Suppressed Rhesus Macaque Model (3R01DA052859-02S1). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10455888. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*