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Abstract
Recently, IgE-independent pathway of mast cell and eosinophil degranulation caused by Mas-related G-protein coupled receptors (MRGPRs) activation has been discovered. It contributes to diseases such as atopic dermatitis, chronic urticaria, and rosacea. Endogenous and exogenous compounds, including substance P, compound 48/80, and somatostatin, can induce itch and inflammation by activating MGRPRs on free nerve endings and mast cells in the skin. In dogs and humans, compound 48/80 degranulates mast cells directly through MRGPR member X2 (MRGPRX2). Compound 48/80 intradermal injection in healthy dogs induced cutaneous allergic reactions in a pilot study; however, the associated activated inflammatory and pruritic pathways in the canine MRGPRX2-induced lesions have not been investigated. The purpose of this study is to characterize the molecular pathways of acute IgE-independent induced skin lesions through MRGPRX2 activation by compound 48/80 in healthy dogs and determine how these correlate to the transcriptome of naturally occurring human and canine atopic dermatitis.