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Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1alpha.

机译:白细胞介素-1α调节人牙龈角质形成细胞中抗菌肽的表达。

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摘要

In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1alpha (IL-1alpha). IL-1alpha is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1alpha might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and beta-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1alpha (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1alpha-inducible AMPs to provide a rapid and robust innate response to microbial infection.
机译:在口腔中,粘膜角质形成细胞部分地通过产生包括防御素,肾上腺髓质素和钙卫蛋白的广谱抗菌肽(AMP)来抵抗细菌感染。许多AMP的表皮角质形成细胞表达响应白介素1α(IL-1alpha)而增加。 IL-1alpha由表皮角质形成细胞产生,并调节细胞分化。为了更好地了解口腔中的先天免疫力,我们试图使用DNA微阵列和Western印迹分析来确定IL-1alpha如何调节人牙龈角质形成细胞(HGK)AMP的表达。来自三名受试者的HGK表达了11种AMP,包括S100A7,S100A8,S100A9,S100A12,分泌型白细胞蛋白酶抑制剂,脂质运载蛋白2(LCN2),胱抑素C和β-防御素2。在表达的AMP中,S100A7,S100A12和LCN2被上调。通过IL-1alpha(诱导型AMPs);其他AMP被认为是构成性的。因此,人牙龈角质形成细胞表达组成型和IL-1α诱导型AMP,以提供对微生物感染的快速而强大的先天反应。

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