Interplays between Nociceptors and Immune Cells; Mast Cells

In response to damage, resident immune cells are activated and blood borne immune cells are recruited to the site of damage. Immune cells also initiate the sensitization of peripheral nociceptors. The immune system also reduces sensitization by producing immune-derived anti-inflammatory and analgesic or proresolution agents. Mast cells are granulated denizen immune cells that are separate into connective tissueand mucosal subtypes and are locate close to capillaries. Mast cells degranulation needs direct interaction between peripheral nerve terminals mast cells, which is indirect by the calcium-dependent cell adhesion molecule N-cadherin. They participate in innate hostdefense and allergic excitations and are de-granulated within a few minutes of an inflammatory reaction, resulting in liberate of bradykinin, histamine and other mediators that association to vasodilation. Once activated by damage, vascular endothelial cells, and immune and immune-related cells such as keratinocytes also synthesize and exude anti-inflammatory cytokines, pro-resolution lipid mediators and opioid peptides to suppress pain. Mast cells are contribute to nociceptor sensitization in a number of contexts and locate close to primary nociceptive neurons. Reported injection of the secretagogue compound 48/80 promotes degranulation of mast cells in the dura and leads to stimulation of meningeal nociceptors. Mast cell degranulation also contributes to the fast onset of nerve growth factor– influenced thermal hyperalgesia. Pelvic pain associated with neurogenic cystitis was removed in mice missing mast cells. Conclusion: Although these findingsdemonstrate that resident mast cells sensitize peripheral nociceptors, it is unclear which chemical mediator(s) branched from mast cells are basic for this effect.