Pyroptosis is a highly inflammatory form of cell death, which uses intracellularly generated pores to destroy electrolyte homeostasis and perform cell death. Gasdermin D, the pore-forming effector protein of pyroptosis, plays a critical role in coordinating membrane lysis and the release of highly inflammatory molecules. Recently, necrosulfonamide as a direct chemical inhibitor of gasdermin D has been confirmed to bind gasdermin D to inhibit pyroptotic cell death. To provide a more effective theoretical guidance for the influence of gasdermin D inhibitors on pyroptosis, we derive a novel PDE model from the genetic level, and study its threshold dynamics in terms of the basic reproduction number $R_0$. It turns out that threshold dynamics is determined by the sign of $R_0-1$. Under some suitable parameters, our numerical simulations show that environmental heterogeneity may increase transmission risk $R_0$ in time periodic environments. We may underestimate $R_0$ if the time average system is used. Based on some published experimental data, the administration of necrosulfonamide maybe strengthen the health condition of patients rapidly, which may become a new strategy to maintain CD4+ T cell counts at a safe level.

细胞凋亡是细胞死亡的一种高度炎症性形式，它利用细胞内产生的孔破坏电解质稳态并执行细胞死亡。Gasdermin D是发烧的致孔效应蛋白，在协调膜裂解和高度炎性分子的释放中起关键作用。最近，已证实坏死磺酰胺作为加德明D的直接化学抑制剂可结合加德明D抑制焦细胞凋亡。为了对加德敏D抑制剂对细胞凋亡的影响提供更有效的理论指导，我们从遗传水平推导了新的PDE模型，并根据基本繁殖数研究了其阈值动态。${\mathrm{[R}}_0$。事实证明，阈值动态取决于${\mathrm{[R}}_0-\mathrm{1个}$。在一些合适的参数下，我们的数值模拟表明环境异质性可能会增加传播风险${\mathrm{[R}}_0$在定期的环境中。我们可能会低估${\mathrm{[R}}_0$如果使用时间平均系统。根据一些已发表的实验数据，使用坏死磺酰胺可能会迅速改善患者的健康状况，这可能成为将CD4 + T细胞计数维持在安全水平的新策略。