Cytokine secretion profile of human keratinocytes exposed to Malassezia yeasts
Cytokine secretion profile of human keratinocytes exposed to Malassezia yeasts
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DOI：
10.1111/j.1574-695x.2006.00163.x
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发表时间：
2006-12-01
影响因子：
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通讯作者：
Nishikawa, Akemi
中科院分区：
文献类型：
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作者：
Ishibashi, Yoshio;Sugita, Takashi;Nishikawa, Akemi
亲脂酵母菌马拉色菌是特应性皮炎（AD）的加重因子。在马拉色菌属的微生物中，球形马拉色菌和限制性马拉色菌在AD患者的皮肤上尤其占优势。然而，马拉色菌在阿尔茨海默病病理生理中的确切作用仍不确定。角质形成细胞通过分泌细胞因子在皮肤炎症和免疫反应中发挥关键作用。在这项研究中，我们试图确定暴露于马拉色菌酵母的人角质形成细胞的细胞因子分泌谱。将人角质形成细胞PHK16-0b与globosa或限制性M.共培养24h，利用细胞因子抗体阵列分析细胞因子分泌谱。角质形成细胞对两种马拉色菌的反应不同。th2型细胞因子谱，即globosa诱导角质形成细胞分泌IL-5、IL-10和IL-13，而限制性M.诱导IL-4分泌。在原代正常人表皮角质形成细胞中获得了类似的结果。cDNA微阵列分析证实，IL-5、IL-10和IL-13 mRNA仅能被球形念珠菌诱导表达，而IL-4 mRNA仅能被限制性念珠菌诱导表达。这些发现表明，球形m.b osa和M * restricta通过刺激Th2免疫应答在触发或加重AD中发挥协同作用。
The lipophilic yeast Malassezia is an exacerbating factor in atopic dermatitis (AD). Among organisms of the Malassezia species, Malassezia globosa and Malassezia restricta are particularly dominant on the skin of AD patients. However, the precise role of Malassezia yeasts in the pathophysiology of AD remains uncertain. Keratinocytes play a critical role in cutaneous inflammatory and immune responses by secreting cytokines. In this study, we attempted to determine the cytokine secretion profiles of human keratinocytes that were exposed to Malassezia yeasts. The human keratinocyte cell line PHK16-0b was cocultivated with M. globosa or M. restricta for 24h, and the resulting cytokine secretion profile was analysed using a cytokine antibody array. The keratinocytes responded to the two Malassezia species with different. Th2-type cytokine profiles, i.e. M. globosa induced IL-5, IL-10 and IL-13 secretion from the keratinocytes, whereas M. restricta induced IL-4 secretion. Similar results were obtained with primary normal human epidermal keratinocytes. cDNA microarray analysis confirmed that IL-5, IL-10, and IL-13 mRNAs were induced only by M. globosa, while IL-4 mRNA expression was induced only by M. restricta. These findings suggest that M. globosa and M * restricta play a synergistic role in triggering or exacerbating AD by stimulating the Th2 immune response.