The C–C chemokines, RANTES and eotaxin, in atopic dermatitis

ONE of the characteristics of atopic dermatitis (AD) skin lesions is an eosinophil in®ltrate and extensive deposition of eosinophil granule proteins in the dermis. RANTES (regulated on activation, normal T expressed and secreted) and eotaxin are potent and well-characterized chemokines for eosinophils (1, 2). In the present study, we determined RANTES and eotaxin contents in the scales obtained from lesional skin with speci®c ELISA systems (R&D Systems). Scales were collected from skin lesions of 15 patients with AD, and six with psoriasis vulgaris. Scales were also collected from four AD patients, who had no obvious lesions in their sole skin, and six healthy donors by scraping their sole skin. RANTES was detected in the lesional scales from all patients with AD studied (12.8u17.8 pg/mg scale), and from ®ve of six patients with psoriasis (4.76u5.46 pg/ mg scale) (Fig. 1a). The concentrations of RANTES were under the detection limit (below 1 pg/mg scale) in the scale extracts from the nonin ̄ammatory skin. The RANTES levels in the scales of AD were signi®cantly higher than those in psoriasis (P.0.05). Eotaxin was detected in the lesional scales of 13 of 14 patients with AD (0.30u0.32 pg/mg scale), whereas the concentrations of eotaxin were under the detection limit (below 0.1 pg/mg scale) in the scale extracts from the patients with psoriasis as well as nonin ̄ammatory skin (Fig. 1b). There was signi®cant correlation between eotaxin content in the scale and blood eosinophil count in the AD patients. However, no signi®cant correlation was seen between RANTES content in the scales and blood eosinophil count. Increased contents of the C-C chemokines, RANTES and eotaxin, were demonstrated in the lesional scales of AD, suggesting the involvement of these chemokines in the pathogenesis of AD. RANTES is known to be produced from epidermal keratinocytes by stimulation with the Th1 cytokine IFN-c, together with proin ̄ammatory cytokines such as TNF-a, IL-1a, and IL-1b (3, 4), suggesting that RANTES in lesional scales is derived from keratinocytes. Eotaxin detected in the lesional scales might be also derived from keratinocytes, because epithelial cells produce eotaxin after stimulation with IL1b and TNF-a. On the other hand, the eotaxin in the scales might be derived from dermal ®broblasts, since dermal ®broblasts produce large amounts of eotaxin after stimulation with IL-4 together with TNF-a (2). Although a relationship between the eotaxin content in the lesional scales and the blood eosinophil count was detected in the patients with AD, it is unlikely that the eotaxin produced in the lesions directly regulates the blood eosinophilia. Production of eotaxin is upregulated by a Th2 cytokine, IL-4 (2), and downregulated by a Th1 Increased levels were found in lesional scales. the children in our series were below the age of 24 months. The second important ®nding of our study is that all the patients allergic to sesame seed had atopic dermatitis. Infants and children with atopic dermatitis are known to have a higher prevalence of food allergy than normal children, with a reported rate of 37% in one study (5). Removal of food allergens such as egg, milk, soybean, and peanuts from the patients' diet can lead to a signi®cant clinical improvement (6). Our ®ndings indicate that allergy to sesame seed is increasing in infants and small children; therefore, sesame seed should be added to the list of allergenic foods in the ®rst year of life. Elimination of sesame seed from the diet should be considered in infants with atopic dermatitis or atopic family history.