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The Inflammatory Response Induced by Aspartic Proteases of Candida albicans Is Independent of Proteolytic Activity

机译：白色念珠菌天冬氨酸蛋白酶诱导的炎症反应与蛋白水解活性无关。

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The secretion of aspartic proteases (Saps) has long been recognized as a virulence-associated trait of the pathogenic yeast Candida albicans. In this study, we report that different recombinant Saps, including Sap1, Sap2, Sap3, and Sap6, have differing abilities to induce secretion of proinflammatory cytokines by human monocytes. In particular Sap1, Sap2, and Sap6 significantly induced interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), and IL-6 production. Sap3 was able to stimulate the secretion of IL-1β and TNF-α. All Saps tested were able to induce Ca2+ influx in monocytes. Treatment of these Saps with pepstatin A did not have any effect on cytokine secretion, indicating that their stimulatory potential was independent from their proteolytic activity. The capacity of Saps to induce inflammatory cytokine production was also independent from protease-activated receptor (PAR) activation and from the optimal pH for individual Sap activity. The interaction of Saps with monocytes induced Akt activation and phosphorylation of IκBα, which mediates translocation of NF-κB into the nucleus. Overall, these results suggest that individual Sap proteins can induce an inflammatory response and that this phenomenon is independent from the pH of a specific host niche and from Sap enzymatic activity. The inflammatory response is partially dependent on Sap denaturation and is triggered by the Akt/NF-κB activation pathway. Our data suggest a novel, activity-independent aspect of Saps during interactions of C. albicans with the host.
机译：天冬氨酸蛋白酶（Saps）的分泌一直被认为是致病性酵母 Candida albicans 的一种毒力相关性状。在这项研究中，我们报道了不同的​​重组Saps，包括Sap1，Sap2，Sap3和Sap6，具有不同的能力来诱导人单核细胞分泌促炎性细胞因子。特别是，Sap1，Sap2和Sap6显着诱导白介素1β（IL-1β），肿瘤坏死因子α（TNF-α）和IL-6产生。 Sap3能够刺激IL-1β和TNF-α的分泌。所有测试的Saps都能诱导单核细胞中Ca 2 + 的流入。用胃抑素A处理这些Saps对细胞因子的分泌没有任何影响，表明它们的刺激潜能与蛋白水解活性无关。 Saps诱导炎性细胞因子产生的能力也独立于蛋白酶激活受体（PAR）的激活以及单个Sap活性的最佳pH。 Saps与单核细胞的相互作用诱导了IktBα的Akt活化和磷酸化，介导了NF-κB向核内的转运。总体而言，这些结果表明，单个Sap蛋白可以诱导炎症反应，并且这种现象与特定宿主环境的pH值和Sap酶活性无关。炎症反应部分取决于Sap变性，并由Akt /NF-κB激活途径触发。我们的数据表明，在 C相互作用期间，Saps具有新颖的，与活性无关的方面。 albicans 与主持人。

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