The Role of Neuropeptides in Psoriasis

R. Saraceno; C.E. Kleyn; G. Terenghi; C.E.M. Griffiths

Disclosures

The British Journal of Dermatology. 2006;155(5):876-882. 

In This Article

Summary and Introduction

Summary

The pathogenesis of psoriasis is incompletely understood but cutaneous neurogenic inflammation is probably involved. This involvement is suggested by a number of clinical and histological observations. Reports about the distribution of cutaneous nerves and the quantification of nerve growth factor and neuropeptides, including calcitonin gene-related peptide and vasoactive intestinal peptide, in lesional and nonlesional psoriatic skin suggest that sensory neuropeptides contribute to the development of psoriasis. This review summarizes what is known about the role of neurogenic markers in psoriasis.

Introduction

Psoriasis is a complex, multifactorial disease whose pathogenesis is not fully elucidated. Clinical observations such as plaque symmetry and stress-induced onset and/or exacerbations suggest a role for the nervous system in the biology of psoriasis.

The symmetrical distribution of plaques in the majority of patients with psoriasis[1] might be explained anatomically by viewing peripheral sensory nerves as constituents of a complex immunomodulatory network.[2] Moreover, the temporal relationship of the onset and/or exacerbation of psoriasis to emotional stress indicates a mechanistic link between the immune and nervous systems, i.e. neurogenic inflammation. Seville[3] observed that the incubation time — between a period of stress and time of flare of psoriasis was typically between 2 days and 1 month in 94% of cases. Anxiety, depression, marital or financial problems, or 'near death' experience have also been identified as triggering factors.[4,5,6] Other clinical correlates include resolution of plaques of psoriasis in areas of denervation secondary to cutaneous nerve transection.[7,8,9]

The role of neuropeptides is underlined by the therapeutic efficacy of neuropeptide-modulating agents such as capsaicin, somatostatin and peptide T.[10] More recently improvement (both clinical and histological) has been observed in a xenotransplant model of psoriasis in severe combined immunodeficient mice treated with K252a, a high-affinity nerve growth factor (NGF) receptor blocker; this observation underscores the relevant role of NGF in this disease.[11] Immunohistochemical studies have revealed a marked proliferation of cutaneous nerves, and presence of substance P (SP), vasoactive intestinal peptide (VIP), protein gene product 9·5 (PGP 9·5), calcitonin gene-related peptide (CGRP) and NGF in plaques of psoriasis ( Table 1 ). In the skin, the ability of neuropeptides to initiate cutaneous inflammation is key to our understanding of their putative role in psoriasis.[12] This review will summarize what is known about the role of neurogenic markers in psoriasis.

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