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Topical glucocorticoid augments scratching behaviour in dinitrofluorobenzene‐sensitized mice by the induction of substance P
Author(s) -
Bae SangJae,
Lee JeongBeom,
Takenaka Motoi,
Tanaka Yoichi,
Shimizu Kazuhiro,
Katayama Ichiro
Publication year - 2004
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/j.0906-6705.2004.00242.x
Subject(s) - scratching , chemistry , allergic contact dermatitis , nitric oxide synthase , tumor necrosis factor alpha , immunology , interleukin , nitric oxide , glucocorticoid , pharmacology , endocrinology , cytokine , medicine , allergy , physics , acoustics
Topical glucocorticoid (GC) is commonly applied in atopic dermatitis treatment. However, the chronic use of GC may be associated with significant side effects. In this study, we investigated whether long‐term epicutaneous application of GC modulates scratching behaviour in dinitrofluorobenzene (DNFB) contact‐sensitized mice. After challenge with DNFB, scratching behaviour was increased in DNFB‐sensitized mice treated with GC in contrast to control mice. In addition, reverse transcriptase‐polymerase chain reaction analysis demonstrated that the expression of preprotachykinin‐A (PPT‐A) mRNA, a precursor of substance P (SP), and inducible nitric oxide synthase (iNOS) mRNA in mice, to which GC was applied, was only observed. In order to evaluate the factors responsible for the augmented scratching behaviour, we injected various cytokines (interleukin‐1α (IL‐1α), IL‐2, IL‐3 and tumour necrosis factor‐α (TNF‐α)) subcutaneously into the ear of DNFB contact‐sensitized mice before DNFB challenge. Among the cytokines, only IL‐3 and TNF‐α significantly increased scratching behaviour in DNFB contact dermatitis mice. Furthermore, PPT‐A mRNA was only expressed in mice pre‐injected with IL‐3 before challenge, but not in those pre‐injected with other cytokines. Taken together, our results suggest that topical GC may augment the itching sensation in DNFB‐sensitized mice through modulation of iNOS and SP induced by IL‐3.