Inflammasomes are multiprotein platforms assembled in the cytosol in response to pathogens and cell stress. Inflammasomes are recognized by their important role on defenses against bacterial infections and have been also implicated in a range of human inflammatory disorders. Intracellular sensors such as NLRP1, NLRP3, NLRC4, AIM2 and Pyrin induce assembly of inflammasomes, while caspase-11 induces the non-canonical pathway for activation of the NLRP3 inflammasome. The formation of the inflammasome leads to caspase-1 activation that triggers pyroptosis and activation of interleukin-1β (IL-1β) and IL-18. Pyroptotic cell death and cytokines production are involved in restriction of bacterial replication by limiting the replication niche of intracellular bacteria and by inducing inflammatory responses. In this review we focus on the mechanisms mediated by inflammasome activation that leads to inflammatory responses and restriction of bacterial infection.

中文翻译：

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涉及感知和限制细菌复制的炎症小体依赖性机制。

炎性体是响应病原体和细胞应激而组装在胞质溶胶中的多蛋白平台。炎症小体因其在防御细菌感染方面的重要作用而得到认可，并且还与一系列人类炎症性疾病有关。细胞内传感器如 NLRP1、NLRP3、NLRC4、AIM2 和 Pyrin 诱导炎症小体的组装，而 caspase-11 诱导激活 NLRP3 炎症小体的非经典途径。炎性体的形成导致 caspase-1 激活，从而引发细胞焦亡和白细胞介素 1β (IL-1β) 和 IL-18 的激活。Pyroptotic 细胞死亡和细胞因子的产生通过限制细胞内细菌的复制生态位和诱导炎症反应参与限制细菌复制。