Analysis of chemical mediators and cytokines in the lesional scales of atopic dermatitis

我们分析了特应性皮炎病变尺度的化学介质和细胞因子。特应性皮炎鳞片组胺含量的测定特应性皮炎病变鳞片组胺含量平均值为1.16±0.85 ng/mg，显著高于健康人群脚底组胺含量（0.16±0.05 ng/mg: p < 0.01）。(1)白细胞介素- (IL-) 6家族细胞因子12例特应性皮炎患者鳞片中IL-6、IL-11、癌抑素M、白血病抑制因子含量分别为8.1±2.5 pg/mg、0.36±7.1 pg/mg和16.6±4.8 pg/mg、0.02±0.04 pg/mg，且IL-6含量与组胺含量相关。这些细胞因子的浓度在非炎症皮肤的鳞片提取物的检测限度之内。(2) C-C趋化因子、RANTES和eotaxin在研究的特应性皮炎患者的皮损鳞片中检测到较多的RANTES和eotaxin （RANTES平均值；12.8±17.8 pg/mg鳞片，eotaxin平均值；0.30±0.32 pg/mg鳞片）。非炎症皮肤鳞片提取物中RANTES和eotaxin的浓度均在检测限内。异应性皮炎患者eotaxin含量与血嗜酸性粒细胞计数有显著相关性，而RANTES含量与血嗜酸性粒细胞计数无显著相关性。RANTES启动子基因多态性-401G/A与冻干性皮炎相关我们研究了日本特应性皮炎受试者的多态性，发现-401A等位基因与特应性皮炎相关。AA、AG、GG基因型分别在特应性皮炎患者10例、33例、22例，健康对照9例、37例、47例。65例日本特应性皮炎患者-401A等位基因频率为0.407，显著高于对照组93例（0.295）。我们在-401A等位基因患者的鳞片中发现了比-401G等位基因患者更多的RANTES蛋白。虽然-401G/A基因型不影响检查数据，如总IgE水平和抗原特异性IgE水平以及血液嗜酸性粒细胞计数，但基因型-401A可能通过在皮肤中产生更多的RANTES而对特应性皮炎易感性。IL-6家族细胞因子IL-6、IL-11、肿瘤抑制素M和白血病抑制因子对肥大细胞生长的影响在肥大细胞/成纤维细胞共培养系统中，这些细胞因子诱导肥大细胞增殖。通过逆转录酶介导的聚合酶链反应，在NIH/3T3成纤维细胞中检测到gp130 mRNA和IL-6家族四成员细胞因子受体，而不是在肥大细胞中检测到。因此，IL-6家族细胞因子可能通过肥大细胞-成纤维细胞相互作用促进皮肤病肥大细胞增生。少

We analyzed the chemical mediators and cytokines in the lesional scales of atopic dermatitis.1. Determination of histamine-contents in scales of atopic dermatitisThe mean histamine content of atopic dermatitis lesional scales was 1.16 ± 0.85 ng/mg scale, and this was significantly higher than that from sole of healthy individuals (0.16 ± 0.05 ng/mg scale : p < 0.01)2. Determination of cytokine-contents in scales of atopic dermatitis(1) Interleukin - (IL-) 6 family cytokinesAmount of IL-6, IL-11, oncostatin M, leukemia inhibitory factor were 8.1 ± 2.5 pg/mg scale, 0.36 ± 7.1 pg/mg scale and 16.6 ± 4.8 pg/mg scale, 0.02 ± 0.04 pg/mg scale, respectively, in the scales obtained from 12 patients with atopic dermatitis, and the amount of IL-6 were correlated with that of histamine in the scales of atopic dermatitis patients. Concentrations of these cytokines were under detection limits in the scale extracts from the non-inflammatory skin.(2) C-C Chemokine, RANTES and eotaxinRANTES and eotaxi … More n RANTES and eotaxin were detected in the lesional scales from the patients with atopic dermatitis studied (mean value of RANTES ; 12.8 ± 17.8 pg/mg scale, mean value of eotaxin ; 0.30 ± 0.32 pg/mg scale). Concentrations of RANTES and eotaxin were under detection limits in the scale extracts from the non-inflammatory skin. There was significant correlation between eotaxin content and blood eosinophil count in atopic dermatitis patients, whereas not in the case with RANTES content.3. RANTES promotor gene polymorphism -401G/A is associated with aspic dermatitisWe investigated the polymorphism in Japanese atopic dermatitis subjects and found that the association of -401A allele with atopic dermatitis. The genotype AA, AG and GG were found in 10, 33, and 22 atopic dermatitis patients, and 9, 37, and 47 healthy controls, respectively. The frequency of -401A allele was 0.407 in 65 Japanese with atopic dermatitis and was significantly higher than that of 93 control subjects (0.295). We found more RANTES protein in the scales obtained from the patients having -401A allele than the patients with -401G allele. Although the -401G/A genotype did not influence the examination data, such as total as well as antigen-specific IgE levels and blood eosinophil count, the genotype -401A might susceptibility to atopic dermatitis by producing more RANTES in skin.4. The IL-6 family cytokines enhance mast cell growth through fibroblast-dependent pathwayWhen the effect of four IL-6 family cytokines, IL-6, IL-11, oncostatin M and leukemia inhibitory factor, were examined on mast cell growth in a mast call/fibroblast co-culture system, these cytokines induced proliferation of the mast cells. mRNA for gp130 and receptors for the four members of IL-6 family cytokines were detected not in mast cells but in NIH/3T3 fibroblasts by reverse transcriptase-mediated polymerase chain reaction. IL-6 family cytokines may thus contribute to mast cell hyperplasia in skin disease through the mast cell-fibroblast interaction. Less