Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can enter the central nervous system and cause several neurological manifestations. Data from cerebrospinal fluid analyses and postmortem samples have been shown that SARS-CoV-2 has neuroinvasive properties. Therefore, ongoing studies have focused on mechanisms involved in neurotropism and neural injuries of SARS-CoV-2. The inflammasome is a part of the innate immune system that is responsible for the secretion and activation of several pro-inflammatory cytokines, such as interleukin-1β, interleukin-6, and interleukin-18. Since cytokine storm has been known as a major mechanism followed by SARS-CoV-2, inflammasome may trigger an inflammatory form of lytic programmed cell death (pyroptosis) following SARS-CoV-2 infection and contribute to associated neurological complications. We reviewed and discussed the possible role of inflammasome and its consequence pyroptosis following coronavirus infections as potential mechanisms of neurotropism by SARS-CoV-2. Further studies, particularly postmortem analysis of brain samples obtained from COVID-19 patients, can shed light on the possible role of the inflammasome in neurotropism of SARS-CoV-2.

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 可进入中枢神经系统并引起多种神经系统表现。脑脊液分析和尸检样本的数据表明，SARS-CoV-2 具有神经侵袭特性。因此，正在进行的研究主要集中在 SARS-CoV-2 的神经趋向性和神经损伤的机制上。炎症小体是先天免疫系统的一部分，负责多种促炎细胞因子的分泌和激活，例如白细胞介素 1β、白细胞介素 6 和白细胞介素 18。由于细胞因子风暴被认为是 SARS-CoV-2 的主要机制，因此炎性体可能在 SARS-CoV-2 感染后引发炎症形式的裂解性程序性细胞死亡（细胞焦亡），并导致相关的神经系统并发症。我们回顾并讨论了冠状病毒感染后炎症小体及其后果焦亡作为 SARS-CoV-2 向神经性的潜在机制的可能作用。进一步的研究，特别是对从 COVID-19 患者身上获得的脑样本进行尸检分析，可以揭示炎症小体在 SARS-CoV-2 趋神经性中的可能作用。