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首页> 外文期刊>Infection and immunity >Signal Transduction and Nuclear Responses in Staphylococcus aureus- Induced Expression of Human β-Defensin 3 in Skin Keratinocytes
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Signal Transduction and Nuclear Responses in Staphylococcus aureus- Induced Expression of Human β-Defensin 3 in Skin Keratinocytes

机译：金黄色葡萄球菌诱导的皮肤角质形成细胞中人β-防御素3表达的信号转导和核反应。

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The human β-defensin 3 (hBD-3) is an inducible epithelial peptide antibiotic that has potent antistaphylococcal activity. Infection of skin epithelial cells with viable Staphylococcus aureus, a common skin pathogen, induces increased gene expression of hBD-3 and other antimicrobial peptides. The aim of this study was to identify signaling pathways and nuclear responses that contribute to the gene expression of hBD-3 in primary human keratinocytes upon contact with S. aureus. Increased hBD-3 peptide was observed by immunofluorescence microscopy in keratinocytes exposed to S. aureus and to lipoteichoic acid (LTA). Both are ligands for the cell surface Toll-like receptor 2 (TLR2), and thus the contribution of TLR2 signaling in hBD-3 expression was examined. Functional inhibition of TLR2 prior to S. aureus stimulation significantly decreased hBD-3 mRNA levels by 37%, attesting to the involvement of this surface receptor in the initial recognition and downstream signaling for hBD-3 expression. Treatment of keratinocytes with a p38 mitogen-activated protein kinase (MAPK) inhibitor prior to either S. aureus or LTA stimulation was associated with reduced hBD-3 mRNA transcripts and peptide. We also propose a role for the MAPK-regulated transcriptional activating protein 1 in S. aureus-induced hBD-3 gene expression. Combined, these studies indicate a role for TLR2 signaling and MAPK activation in the upregulation of hBD-3 and demonstrate the innate immune capacity of skin keratinocytes under conditions of S. aureus challenge to enhance the local expression of this antistaphylococcal peptide antibiotic.
机译：人β-防御素3（hBD-3）是一种可诱导的上皮肽抗生素，具有有效的抗葡萄球菌活性。活的金黄色葡萄球菌（一种常见的皮肤病原体）感染皮肤上皮细胞会诱导hBD-3和其他抗菌肽的基因表达增加。这项研究的目的是确定与 S接触后有助于原代人角质形成细胞中hBD-3基因表达的信号通路和核反应。金黄色。通过免疫荧光显微镜观察到暴露于 S的角质形成细胞中hBD-3肽增加。金黄色葡萄球菌和脂蛋白酸（LTA）。两者都是细胞表面Toll样受体2（TLR2）的配体，因此检查了TLR2信号在hBD-3表达中的作用。在 S之前对TLR2进行功能抑制。金黄色葡萄球菌刺激显着降低了hBD-3 mRNA水平达37％，证明该表面受体参与了hBD-3表达的最初识别和下游信号传导。在任一时间之前，先用p38丝裂原激活的蛋白激酶（MAPK）抑制剂治疗角质形成细胞。金黄色或LTA刺激与hBD-3 mRNA转录和肽减少有关。我们还提出了在 S中MAPK调节的转录激活蛋白1的作用。金黄色葡萄球菌诱导的hBD-3基因表达结合起来，这些研究表明TLR2信号传导和MAPK激活在hBD-3的上调中发挥了作用，并证明了在 S条件下皮肤角质形成细胞的先天免疫能力。金黄色葡萄球菌增强了这种抗葡萄球菌肽抗生素的局部表达。

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