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首页> 外文期刊>Infection and immunity >Mechanisms of Inflammasome Activation by Vibrio cholerae Secreted Toxins Vary with Strain Biotype
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Mechanisms of Inflammasome Activation by Vibrio cholerae Secreted Toxins Vary with Strain Biotype

机译：霍乱弧菌分泌毒素激活炎性体的机制因菌株生物型而异

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Activation of inflammasomes is an important aspect of innate immune responses to bacterial infection. Recent studies have linked Vibrio cholerae secreted toxins to inflammasome activation by using murine macrophages. To increase relevance to human infection, studies of inflammasome-dependent cytokine secretion were conducted with the human THP-1 monocytic cell line and corroborated in primary human peripheral blood mononuclear cells (PBMCs). Both El Tor and classical strains of V. cholerae activated ASC (apoptosis-associated speck-like protein-containing a CARD domain)-dependent release of interleukin-1β (IL-1β) when cultured with human THP-1 cells, but the pattern of induction was distinct, depending on the repertoire of toxins the strains produced. El Tor biotype strains induced release of IL-1β dependent on NOD-like receptor family pyrin domain-containing 3 (NLRP3) and ASC due to the secreted pore-forming toxin hemolysin. Unlike in studies with mouse macrophages, the MARTX toxin did not contribute to IL-1β release from human monocytic cells. Classical biotype strains, which do not produce either hemolysin or the MARTX toxin, activated low-level IL-1β release that was induced by cholera toxin (CT) and dependent on ASC but independent of NLRP3 and pyroptosis. El Tor strains likewise showed increased IL-1β production dependent on CT when the hemolysin gene was deleted. In contrast to studies with murine macrophages, this phenotype was dependent on a catalytically active CT A subunit capable of inducing production of cyclic AMP and not on the B subunit. These studies demonstrate that the induction of the inflammasome in human THP-1 monocytes and in PBMCs by V. cholerae varies with the biotype and is mediated by both NLRP3-dependent and -independent pathways.
机译：炎性小体的激活是对细菌感染的固有免疫反应的重要方面。最近的研究已经通过使用鼠巨噬细胞将霍乱弧菌分泌的毒素与炎症小体活化联系起来。为了增加与人类感染的相关性，使用人类THP-1单核细胞系进行了炎症小体依赖性细胞因子分泌的研究，并在人类原代外周血单核细胞（PBMC）中得到证实。当与人THP-1细胞培养时，El Tor和霍乱弧菌的经典菌株均激活了ASC（细胞凋亡相关的斑点样蛋白质，含有CARD域）依赖性白细胞介素1β（IL-1β）的释放，但模式诱导的方式是不同的，取决于菌株产生的毒素种类。由于分泌的成孔毒素溶血素，El Tor生物型菌株诱导依赖于含NOD样受体家族含3个pyrin域的蛋白（A1）和ASC的IL-1β释放。与小鼠巨噬细胞研究不同，MARTX毒素不会促进人单核细胞释放IL-1β。不产生溶血素或MARTX毒素的经典生物型菌株激活由霍乱毒素（CT）诱导并依赖于ASC但不依赖NLRP3和发烧的低水平IL-1β释放。当删除溶血素基因时，El Tor菌株同样显示出依赖于CT的IL-1β产生增加。与鼠类巨噬细胞研究相反，该表型取决于能够诱导环状AMP产生的催化活性CT A亚基，而不取决于B亚基。这些研究表明，霍乱弧菌对人THP-1单核细胞和PBMC中炎症小体的诱导随生物型而变化，并由NLRP3依赖性和非依赖性途径介导。

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