Abstract
Mast cells (MCs) are immune cells and are widely distributed throughout the body. MCs are not only classically viewed as effector cells of some allergic diseases but also participate in host defense, innate and acquired immunity, homeostatic responses, and immunoregulation. Mounting evidence indicates that activation of MCs releasing numerous vasoactive and inflammatory mediators has effects on the nervous system and has been involved in different pain conditions. Here, we review the latest advances made about the implication of MCs in pain. Possible cellular and molecular mechanisms regarding the crosstalk between MC and the nervous system in the initiation and maintenance of pain are also discussed.
Highlights
Pain is a hallmark of inflammation that can be either protective or detrimental during acute or chronic stages
Considerable evidence suggests that mast cells (MCs), effectors of innate immunity and local inflammation, regulate pain signaling, for example, by secreting mediators that activate nearby nerves based on their histological proximity (Chompunud Na Ayudhya et al, 2020; AguileraLizarraga et al, 2021)
The results indicate that MCs play an important role in different painful conditions, some studies showed that depletion or stabilization of MC did not display pain-relieving effect in models induced by complete Freund’s adjuvant, carrageenan, formalin, nerve growth factor (NGF), or nociceptin/orphanin (McDougall and Larson, 2006; Xanthos et al, 2011; Lopes et al, 2017; Magnusdottir et al, 2018)
Summary
Reviewed by: Albert Rizvanov, Kazan Federal University, Russia Rossella Paolini, Sapienza University of Rome, Italy. Mast cells (MCs) are immune cells and are widely distributed throughout the body. MCs are classically viewed as effector cells of some allergic diseases and participate in host defense, innate and acquired immunity, homeostatic responses, and immunoregulation. Mounting evidence indicates that activation of MCs releasing numerous vasoactive and inflammatory mediators has effects on the nervous system and has been involved in different pain conditions. We review the latest advances made about the implication of MCs in pain. Possible cellular and molecular mechanisms regarding the crosstalk between MC and the nervous system in the initiation and maintenance of pain are discussed
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