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首页> 外文期刊>Infection and immunity >Induction of Caspase-11 by Aspartyl Proteinases of Candida albicans and Implication in Promoting Inflammatory Response
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Induction of Caspase-11 by Aspartyl Proteinases of Candida albicans and Implication in Promoting Inflammatory Response

机译：白色念珠菌天冬氨酰蛋白酶诱导Caspase-11的表达及其对炎症反应的促进作用

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We recently demonstrated that the secreted aspartyl proteinases (Saps), Sap2 and Sap6, of Candida albicans have the potential to induce the canonical activation of the NLRP3 inflammasome, leading to the secretion of interleukin-1β (IL-1β) and IL-18 via caspase-1 activation. We also observed that the activation of caspase-1 is partially independent from the NLRP3 activation pathway. In this study, we examined whether Sap2 and Sap6 are also able to activate the noncanonical inflammasome pathway in murine macrophages. Our data show that both Sap2 and Sap6 can activate caspase-11 through type I interferon (IFN) production. Caspase-11 cooperates to activate caspase-1, with a subsequent increase of IL-1β secretion. Endocytosis and internalization of Saps are required for the induction of type I IFN production, which is essential for induction of noncanonical inflammasome activation. Our study indicates a sophisticated interplay between caspase-1 and caspase-11 that connects the canonical and noncanonical pathways of inflammasome activation in response to C. albicans Saps.
机译：我们最近证明，白色念珠菌的分泌的天冬氨酰蛋白酶（Saps），Sap2和Sap6具有诱导NLRP3炎性体正常激活的潜力，从而导致白介素1β（IL-1β）和IL-18的分泌通过caspase-1激活。我们还观察到caspase-1的激活部分独立于NLRP3激活途径。在这项研究中，我们检查了Sap2和Sap6是否还能够激活鼠巨噬细胞中的非典型炎症小体途径。我们的数据显示Sap2和Sap6均可通过I型干扰素（IFN）产生激活caspase-11。 Caspase-11协同激活caspase-1，随后IL-1β分泌增加。诱导I型IFN的产生需要Saps的胞吞作用和内在化作用，这对于诱导非规范性炎症小体激活至关重要。我们的研究表明，caspase-1和caspase-11之间存在复杂的相互作用，可连接响应白色念珠菌的炎症小体激活的规范和非规范途径。

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