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首页> 外文期刊>Infection and immunity >Released ATP Is an Extracellular Cytotoxic Mediator in Salivary Histatin 5-Induced Killing of Candida albicans
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Released ATP Is an Extracellular Cytotoxic Mediator in Salivary Histatin 5-Induced Killing of Candida albicans

机译：释放的ATP是唾液组蛋白5致白色念珠菌致死中的细胞外细胞毒性介质。

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Salivary histatins (Hsts) are antifungal peptides with promise as therapeutic agents against candidiasis. Hst 5 kills the fungal pathogenCandida albicans via a mechanism that involves release of cellular ATP in the absence of cytolysis. Here we demonstrate that released ATP has a further role in Hst 5 killing. Incubation of the cells with ATP analogues induced cell death, and addition of the ATP scavenger apyrase to remove extracellular ATP released during Hst 5 treatment resulted in a reduction in cell killing. Experiments using anaerobically grown C. albicans with decreased susceptibility to Hst 5 confirmed that depletion of cellular ATP as a result of ATP efflux was not sufficient to cause cell death. In contrast to Hst-susceptible aerobic cultures, anaerobically grown cells were not killed by exogenously applied ATP. These findings established that Hst binding, subsequent entry into the cells, and ATP release precede the signal for cytotoxicity, which is mediated by extracellular ATP. In a higher-eukaryote paradigm, released ATP acts as a cytotoxic mediator by binding to membrane nucleotide P2X receptors. Based on a pharmacological profile and detection of a C. albicans60-kDa membrane protein immunoreactive with antibody to P2X7 receptor, we propose that released ATP in response to Hst 5 activates candidal P2X7-like receptors to cause cell death.
机译：唾液组蛋白（Hsts）是抗真菌肽，有望作为抗念珠菌病的治疗剂。 Hst 5通过一种在没有细胞溶解的情况下释放细胞ATP的机制杀死真菌病原体白色念珠菌。在这里，我们证明了释放的ATP在Hst 5杀伤中具有进一步的作用。将细胞与ATP类似物一起孵育可诱导细胞死亡，并添加ATP清除剂腺苷三磷酸消除在Hst 5处理过程中释放的细胞外ATP导致细胞杀伤力降低。使用厌氧生长的C进行的实验。 Hst 5敏感性降低的白色念珠菌证实，ATP流出导致细胞ATP耗竭不足以导致细胞死亡。与Hst敏感的需氧培养相比，厌氧培养的细胞不会被外源施加的ATP杀死。这些发现确定了Hst结合，随后进入细胞和ATP释放先于细胞毒性信号，该信号由细胞外ATP介导。在高等真核生物的范例中，释放的ATP通过与膜核苷酸P2X受体结合而充当细胞毒性介质。基于药理学特征和 C的检测。白色念珠菌 60-kDa膜蛋白与P2X 7 受体的抗体发生免疫反应，我们认为释放的ATP响应Hst 5激活了念珠菌P2X 7 样受体。导致细胞死亡。

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