Abstract
Abstract Contact hypersensitivity (CHS) is an experimental model of human allergic contact dermatitis, one of the representative skin diseases, where NLRP3 inflammasome plays a crucial role. Although the regulation of NLRP3 inflammasome activity by cannabinoid 1 receptor (CB1R) has been shown in metabolic diseases such as obesity and type 2 diabetes, the role of CB1R in CHS is unclear. Here, we investigate the putative role of CB1R in CHS by using a selective CB1R antagonist rimonabant. Pharmacological blockade of CB1R by rimonabant ameliorated oxazolone-induced CHS by suppressing hyperproliferation of keratinocytes and expression of pro-inflammatory cytokines in a TLR2/4-dependent manner. The inhibitory effect of rimonabant in oxazolone-induced CHS was not observed in NLRP3-deficient mice. These results suggest that CB1R could control TLR2/4 signaling pathway via NLRP3 inflammasome in CHS. Supported by Basic Science Research Program through the National Research Foundation of Korea(NRF) funded by the Ministry of Education (NRF-2022R1I1A1A01071661)
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