Gouin O, Lebonvallet N, L'Herondelle K, Le Gall-Ianotto C, Buhé V, Plée-Gautier E, Carré JL, Lefeuvre L, Misery L, et al.
Experimental dermatology. Date of publication 2015 Oct 1;volume 24(10):723-6.
1. Exp Dermatol. 2015 Oct;24(10):723-6. doi: 10.1111/exd.12798. Epub 2015 Aug 21.
Self-maintenance of neurogenic inflammation contributes to a vicious cycle in
skin.
Gouin O(1)(2), Lebonvallet N(1), L'Herondelle K(1), Le Gall-Ianotto C(1), Buhé
V(1), Plée-Gautier E(1), Carré JL(1), Lefeuvre L(2), Misery L(1).
Author information:
(1)University of Western Brittany, Laboratory of Neurosciences of Brest, Brest,
France.
(2)Uriage Dermatological Laboratories, Courbevoie, France.
Comment in
Exp Dermatol. 2015 Oct;24(10):732-3.
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 (GPCRs) 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.
© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
DOI: 10.1111/exd.12798
PMID: 26178975 [Indexed for MEDLINE]
