title: Serum levels of Th2 chemokines, CCL17, CCL22, and CCL27, were the important markers of severity in infantile atopic dermatitis.
abstract: Atopic dermatitis (AD) is considered to be Th2 cell-mediated disorder. In most infants with AD, AD may be induced by food allergy. In the early stage of infantile AD, it is unclear whether there are changes in serum Th2 chemokines or in Th2 chemokine production by peripheral blood mononuclear cells (PBMC). Thirty-four patients with AD were examined (mean age, 4.5 months; female:male, 18:16). Ten age-matched infants with no history of allergic disease were used as controls. Thirty of these 34 patients were sensitized with ovalbumin (OVA; radioallergrosolvent score of >2). Serum levels of CCL17, CCL22, and CCL27 were measured with enzyme-linked immunosolvent assay (ELISA) kits and their correlation with the severity of skin lesions, defined by the scoring atopic dermatitis (SCORAD) index, was analyzed. The amounts of TNF-alpha, CCL17, CCL22, and CCL27 in the culture supernatants of PBMC from OVA-sensitized AD infants after stimulation with OVA were estimated with ELISA kits. Elevated serum CCL17, CCL22, and CCL27 levels significantly correlated with SCORAD index (r = 0.7181, p < 0.001; r = 0.5354, p < 0.005; r = 0.8312, p < 0.0001, respectively). CCL22 levels produced by PBMC from OVA-sensitized infants with AD reflected serum CCL22 levels. Only six of 30 OVA-sensitized patients in whom the skin signs increased immediately after OVA intake showed markedly high titers of TNF-alpha produced by PBMC after stimulation with OVA. These high TNF-alpha titers correlated significantly with serum CCL27 levels (r = 0.7181, p < 0.001). Serum concentrations of CCL17, CCL22, and CCL27 correlate well with the extent and intensity of AD in infants. Of the three Th2 chemokines examined, serum CCL27 correlated most significantly with the severity of AD. Thus, the peripheral immune responses of infantile AD patients are skewed to a Th2 dominant bias.
authors.affiliation: Department of Pediatrics, Ohashi Hospital, Toho University Medical Center, Tokyo, Japan.
authors.forename: Junko
authors.initials: J
authors.lastname: Nakazato
authors.forename: Masaru
authors.initials: M
authors.lastname: Kishida
authors.forename: Rei
authors.initials: R
authors.lastname: Kuroiwa
authors.forename: Junko
authors.initials: J
authors.lastname: Fujiwara
authors.forename: Makiko
authors.initials: M
authors.lastname: Shimoda
authors.forename: Noriaki
authors.initials: N
authors.lastname: Shinomiya
mesh_terms: D015415:Biomarkers / Q000097:blood; D054414:Chemokine CCL17 / Q000097:blood*; D054422:Chemokine CCL22 / Q000097:blood*; D054425:Chemokine CCL27 / Q000097:blood*; D003876:Dermatitis, Atopic / Q000175:diagnosis* / Q000276:immunology; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D012720:Severity of Illness Index; D018418:Th2 Cells / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; C106230:CCL17 protein, human; C515482:CCL22 protein, human; C492276:CCL27 protein, human; D054414:Chemokine CCL17; D054422:Chemokine CCL22; D054425:Chemokine CCL27; D014409:Tumor Necrosis Factor-alpha