ArticlebioRxiv : the preprint server for biology2024
Mast cell-derived chymases are essential for the resolution of inflammatory pain in mice.
Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Immune cells play a critical role in the transition from acute to chronic pain. However, the role of mast cells in pain remains under-investigated. Here, we demonstrated that the resolution of inflammatory pain is markedly delayed in mast-cell-deficient mice. In response to Complete Freund Adjuvant (CFA), mast-cell-deficient mice showed greater levels of nitric oxide and altered cytokine/chemokine profile in inflamed skin in both sexes. In Wild-Type (WT) mice, the number of mast cell and mast cell-derived chymases; chymase 1 (CMA1) and mast cell protease 4 (MCPT4) increased in the inflamed skin. Inhibiting chymase enzymatic activity delayed the resolution of inflammatory pain. Consistently, local pharmacological administration of recombinant CMA1 and MCPT4 promoted the resolution of pain hypersensitivity and attenuated the upregulation of cytokines and chemokines under inflammation. We identified CCL9 as a target of MCPT4. Inhibition of CCL9 promoted recruitment of CD206 Summary: Mast cell-derived chymases play an unexpected role in the resolution of inflammatory pain and regulate the immune response. Graphical abstract:
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