Delta-9-tetrahydrocannabinol alleviates inflammation by modulating immune responses in LPS-induced murine inflammation model.

Tomer S.; Harding J.; Wang L.; Kedia N.; Cook E.; Le V.; Platt C.; Le J.; Tien N.; Patalay K. et al. · Frontiers in immunology · 2026

**Background & Methods** This review integrated transcriptomic, cellular, and in vivo approaches to characterize THC's immunomodulatory effects on LPS-induced inflammation. The study employed human THP-1 monocytic cells, primary human monocytes, and a murine model of systemic inflammation, with analysis of inflammatory pathways, gene expression, and immune cell activation markers across multiple biological systems. **Key Findings** • THC suppressed LPS-induced pro-inflammatory responses, including marked reduction of type I interferon-stimulated genes (ISGs) and pro-inflammatory cytokines IL-1β and TNF-α, while simultaneously inducing stress-adaptive transcriptional programs through upregulation of unfolded protein response (UPR) and autophagy pathways in human monocytic cells. • In primary human monocytes and splenic immune populations, THC significantly reduced expression of monocyte activation markers (CD80, CD83, CD209) and attenuated both myeloid and T-cell activation in mice exposed to systemic inflammation. • Brain transcriptomic analysis revealed that chronic THC exposure reduced neuroinflammatory pathway expression while enriching pathways associated with neurogenesis and synaptic plasticity, suggesting neuroprotective effects alongside peripheral immunomodulation. **Dosage & Administration** Not reported. **Safety & Adverse Effects** Not reported. **Evidence Quality** As a 2026 review article, this study provides mechanistic insights through multiple complementary methodologies (transcriptomics, cellular assays, and in vivo models) across human and murine systems, strengthening evidence consistency. However, critical limitations include: (1) reliance on model systems that may not fully recapitulate clinical inflammation; (2) absence of reported dosing information limiting translational application; (3) no adverse effects documentation; and (4) review-based classification suggesting synthesis of existing evidence rather than novel empirical data. The breadth of approach enhances mechanistic understanding, but clinical translation remains preliminary. Further investigation in human clinical trials is warranted before therapeutic recommendations can be established for chronic inflammatory and neuroimmune disorders.

More recent cannabis research