Abstract
Abstract Pain is a cardinal component of inflammation and a significant public health issue. Inflammatory cytokines such as TNF-alpha, IL-1beta, CXCL1/IL-8, as well as neutrophil influx have been implicated in the potentiation of peripheral inflammatory pain in models of thermal and mechanical hindpaw hypernociception in rodents.. Degranulation of mast cells has been shown to be important for phosphorylation of Erk in nociceptive neurons in a rat model of migraine-like stimulation. Mechanical bladder pain in a model of interstitial cystitis was abrogated in mast cell deficient mice. We show that degranulation of plantar mast cells caused by direct secretagogue treatment or passive antibody sensitization and challenge, causes reduction in paw withdrawal latencies as well as significant edema, neutrophil influx, and upregulation of local TNF-alpha and IL-1beta levels, as well as histamine release in the hindpaws of mice in a model of thermal pain. Mast cell-deficient C57BL/6 Wsh/Wsh mice show no edema, histamine release or pain response indicated by reduction in paw withdrawal latencies. This suggests that while pain is a complex and multifactorial physiology, tissue sentinel mast cells may be a critical initiator of inflammatory pain in both protective and allergic/pathological contexts.
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