Defective sweating responses in atopic dermatitis.

While sweat is thought to be one of the important factors provoking exacerbations of clinical symptoms in atopic dermatitis (AD), little attention has been drawn to a beneficial role of sweat in the development of AD lesions. However, if the permeability barrier and antimicrobial barrier dysfunction represents the primary event in the development of AD, an evaluation of sweating responses in AD is a logical place to look for changes that predispose to the disease. In this regard, there have been conflicting data regarding whether sweating responses are impaired, normal or enhanced in AD patients. Consistent with the results of most recent studies, our recent study showed that most AD patients exhibit a defective ability to deliver sweat to the skin surface in response to thermal stress. Despite such defective sweating responses observed in the most part, a marked augmentation in the sweating response with delayed kinetics can be paradoxically detected in some sweating glands of these AD patients, indicating compensatory hyperhidrosis. Dermcidin, a new antimicrobial peptide exclusively produced by sweat glands, was abundantly detected not only in the sweat glands and ducts, and the lumen, but also in the dermal tissues adjacent to the sweat glands. These results indicate that the sweat may be retained in the lumen or pour into the dermal tissues, thereby causing inflammation. Thus, chronic inflammation in AD may be caused in part by a dysfunction of the sweat delivery system.