The innate immune system provides the host with both a dynamic barrier to prevent infection and a means to which rapid anti-microbial responses can be mounted. The inflammasome pathway is a critical host early response mechanism that enables detection of pathogens and initiates production of inflammatory cytokines, inducing recruitment of effector cells to the site of infection. The complete mechanism of inflammasome activation requires two signals: an initial priming step upon detection of pathogen, followed by activation of intracellular pattern recognition receptors critical to the formation of the inflammasome complex. The inflammasome complex is made of intracellular multiprotein oligomers which includes a sensor protein such as the nucleotide-binding oligomerization domain (NOD) like receptor proteins (NLRP), and an adapter protein, ASC, which critically activates pro-caspase-1. The mature caspase-1 then proteolytically cleaves cytosolic pro-IL-1β and pro-IL-18, which are then secreted as inflammatory cytokines that activate the inflammatory arm of the immune response to infection. Active caspase-1 also results in pyroptosis, which is a form of cell death triggered by inflammation. The induction and activation of IL-1β and IL-18 are considered critical signatures for inflammasome activation. With focus upon influenza A virus infection, this review will address present knowledge on the mechanisms of inflammasome complex activation, particularly how the viral components modulate activation of the cytosolic NOD-like receptor protein-3 (NLRP3)-dependent inflammasome complex. We also discuss potential therapeutic strategies that target the inflammasome to ameliorate illness, as well as novel methods of vaccination that target inflammasome stimulation with the aim to increase efficacy.

先天性免疫系统为宿主提供了防止感染的动态屏障，并为宿主提供了快速的抗微生物反应的手段。炎性体途径是关键的宿主早期反应机制，能够检测病原体并启动炎性细胞因子的产生，从而诱导效应细胞募集到感染部位。炎性体激活的完整机制需要两个信号：检测病原体时的初始启动步骤，然后激活对炎性体复合物形成至关重要的细胞内模式识别受体。炎症小体复合物由细胞内多蛋白寡聚体组成，其中包括传感器蛋白，例如受体结合蛋白（NLRP）之类的核苷酸结合寡聚域（NOD），以及衔接子蛋白ASC，关键地激活前胱天蛋白酶-1。然后成熟的半胱天冬酶1蛋白水解地裂解胞质的前IL-1β和前IL-18，然后将它们分泌为激活激活感染免疫反应的炎症分支的炎性细胞因子。活跃的caspase-1也导致焦磷酸化，这是由炎症触发的细胞死亡的一种形式。IL-1β和IL-18的诱导和激活被认为是炎性体激活的关键特征。本文着眼于甲型流感病毒感染，将着眼于炎症小体复合物激活机制的当前知识，特别是病毒成分如何调节依赖于胞质NOD样受体蛋白3（NLRP3）的炎症小体复合物的激活。我们还将讨论针对炎症小体改善疾病的潜在治疗策略，