Abstract
Background: Neuropeptides are considered to be factors that trigger, exacerbate or modulate allergic diseases and inflammatory skin reactions. In addition, it has been indicated that allergic diseases are highly correlated with stress.
Methods: 2,4,6-Trinitrochlorbenzene (TNCB) and crowding stress were applied to mouse atopic dermatitis (AD) models for the purpose of provoking chronic dermatitis. In addition, TNCB-sensitized mice were given olopatadine hydrochloride (10 or 3mg/kg), an anti-allergic agent, orally. The neuropeptide content in the skin tissues and serum IgE levels were measured in these mice.
Results: Repeated local application of TNCB solution induced itching skin lesions, together with an increase in levels of substance P, a decrease in calcitonin gene-related peptide levels and early augmentation of IgE production. Treatment with crowding stress brought about a transient increase in substance P. Furthermore, we observed significant decreases in substance P and serum IgE levels when the administration of olopatadine hydrochloride was started before the elicitation of chronic dermatitis caused by repeated application of TNCB solution. These changes were more definite in the group administered a higher dose of the drug (10mg/kg).
Conclusions: It is suggested that repeated contact allergic dermatitis or mental stress may promote the development and exacerbation of AD and that substance P has a role in this response. In addition, it seems that an anti-allergic drug, such as olopatadine hydrochloride, possibly downregulates substance P, thereby suppressing the development of AD. In the future, the development and clinical application of a drug that strongly influences the release of neuropeptides, such as substance P, and the expression of neuropeptide receptors would be expected for the treatment of AD.
