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细胞焦亡在结核分枝杆菌中研究进展
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Abstract:
焦亡是一种新兴的细胞内在死亡机制，是一种通过依靠半胱氨酸天冬氨酸蛋白酶(caspase)家族的促炎细胞死亡模式，当外来信号刺激被感染细胞时，模式识别受体(pattern recognition receptor, PRR)被自动激活并参与形成炎性小体(NLRP3小体)，NLRP3小体特异性识别切割半胱天冬氨酸(Pro caspase-1/4/5/11)形成成熟的半胱天冬氨酸，继而作用于Gasdermin-D蛋白将其分子的GSDMD-N端解聚嵌入细胞膜上形成内径10~15 nm非选择性孔洞，导致细胞渗透肿胀和裂解坏死，同时将活化的致炎因白细胞介素-1β和IL-18释放到胞外，并募集更多的炎症细胞以此扩大炎症反应。本文就细胞焦亡的分子机制及调控结核分枝杆菌感染后巨噬细胞焦亡的影响因子进行综述。
Pyroptosis is an emerging mechanism of intracellular death. It is a pro-inflammatory cell death mode that relies on the cysteine aspartate protease (caspase) family. When the infected cells are stimulated by foreign signals, pattern recognition receptor (PRR) is automatically activated and participates in the formation of inflammasome (NLRP3 body), which specifically recognizes and clews Pro caspase-1/4/5/11 to form mature caspase. Then, it acts on Gasdermin-D protein to embed the GSDMD-N terminal of its molecule into the cell membrane to form a non-selective hole with an inner diameter of 10~15 nm, resulting in cell infiltration swelling and lysis necrosis. Meanwhile, it releases the activated inflammatory cause interleukin-1β and IL-18 into the extracellular space, and recruits more inflammatory cells to expand the inflammatory response. This article reviews the molecular mechanism of pyroapoptosis and the influencing factors of macrophage pyroapoptosis after mycobacterium tuberculosis infection.
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