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首页> 外文期刊>Journal of dermatological science >The expression of beta-defensin-2, 3 and LL-37 induced by Candida albicans phospholipomannan in human keratinocytes.
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The expression of beta-defensin-2, 3 and LL-37 induced by Candida albicans phospholipomannan in human keratinocytes.

机译：白色念珠菌磷酸脂甘露聚糖诱导的人角质形成细胞中β-defensin-2、3和LL-37的表达。

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摘要

Antimicrobial peptides (AMPs) like beta-defensin-2, 3 and LL-37 are expressed in skin exposed to a variety of stimuli. AMPs play an important role not only in host defense against the invading pathogens, but also in wound healing, release of chemokines and pro-inflammatory cytokines [1,2]. Lopez-Garcia et al. have shown that the expression of LL-37 was upregulated in the skin lesion of Candida albicans infection [3]. The production of beta-defensin-2 in vaginal epithelial cells could be triggered by C. albicans [4]. However, the role of the interaction between human keratinocytes and C. albicans components in the production of AMPs remains unclear. Here, we investigated whether the exposure of human keratinocytes to native phospholipomannan form the cell wall of C. albicans (PLM) could lead to the release of beta-defensin-2,3 and LL-37 and to determine the underlying mechanisms.
机译：像β-防御素2、3和LL-37这样的抗菌肽（AMP）在暴露于各种刺激的皮肤中表达。 AMP不仅在宿主防御入侵病原体方面起着重要作用，而且在伤口愈合，趋化因子释放和促炎性细胞因子中也发挥着重要作用[1,2]。 Lopez-Garcia等。已有研究表明LL-37的表达在白色念珠菌感染的皮肤病变中被上调[3]。白色念珠菌可触发阴道上皮细胞中β-防御素2的产生[4]。但是，人类角质形成细胞和白色念珠菌成分之间的相互作用在AMPs产生中的作用尚不清楚。在这里，我们调查了人类角质形成细胞暴露于天然磷脂酰甘露聚糖是否形成白色念珠菌（PLM）的细胞壁，从而导致β-防御素-2,3和LL-37的释放并确定其潜在机制。

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