C ol~ lponent~ of the cutaneous,~ ervol's system interact WIth multIple types of cells U1 thc skin to mediate actions important in skin inflammation and wound healing [1-5]. Ovcr 100 years ago it was observed that antidromic stimulation of thc scnsory nerves emanating from dorsal root ganglia produced vasodilation and apparcnt local inflammation of the skin (for review see [6]). This observation, repeated many times since, led to the understanding that the cutaneous sensory nervous system (CSNS) not only relays sensory information from the skin to the central nervous system (CNS), but also plays an effector role in the skin's inflammatory. responsc [7-9].

Scnsory neurons express at least 17 different neuropeptides [6]. Several of these, substance P (SP)[6, 10, 11], calcitonin gene-related peptide (CGRP)[12-14], substancc K (SK)[10, 15, 16], and vasoactive intestinal polypeptide fl7-20], havc activities or cellular localizations that suggest involvement" in tissue repair. SP is the prototype of neuropeptidcs releascd from sensory C-fibers in the skin [21]. The activities ofSP require not only secretion but also the expression of the SP rcceptor (SPIt) on local target cells and expression of tissue proteascs that degrade neuropeptides, such as neutral endopeptidase (NEP).