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Self‐maintenance of neurogenic inflammation contributes to a vicious cycle in skin
Author(s) -
Gouin Olivier,
Lebonvallet Nicolas,
L'Herondelle Killian,
Le GallIanotto Christelle,
Buhé Virginie,
PléeGautier Emmanuelle,
Carré JeanLuc,
Lefeuvre Luc,
Misery Laurent
Publication year - 2015
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12798
Subject(s) - inflammation , receptor , proteases , microbiology and biotechnology , neurogenic inflammation , neuroscience , nerve growth factor , immunology , medicine , biology , neuropeptide , substance p , biochemistry , enzyme
Cutaneous neurogenic inflammation ( CNI ) is frequently associated with skin disorders. CNI is not limited to the retrograde signalling of nociceptive sensory nerve endings but can instead be regarded as a multicellular phenomenon. Thus, soluble mediators participating in communication among sensory nerves, skin and immune cells are key components of CNI . These interactions induce the self‐maintenance of CNI , promoting a vicious cycle. Certain G protein‐coupled receptors ( GPCR s) play a prominent role in these cell interactions and contribute to self‐maintenance. Protease‐activated receptors 2 and 4 ( PAR ‐2 and PAR ‐4, respectively) and Mas‐related G protein‐coupled receptors (Mrgprs) are implicated in the synthesis and release of neuropeptides, proteases and soluble mediators from most cutaneous cells. Regulation of the expression and release of these mediators contributes to the vicious cycle of CNI . The authors propose certain hypothetical therapeutic options to interrupt this cycle, which might reduce skin symptoms and improve patient quality of life.