胞浆
膜
膜曲率
上睑下垂
脂多糖
细菌外膜
胶束
生物物理学
细胞生物学
生物
炎症体
脂质A
小泡
血浆蛋白结合
脂质双层
化学
生物化学
细胞膜
结合位点
膜蛋白
蛋白质结构
糖蛋白
膜糖蛋白
生物膜
脂锚定蛋白
作者
Jakub Began,Alexandra Boegli,Leonie Anton,Denys Biriukov,Juvan Vairamuthu,José Carlos Santos,Petr Brož
出处
期刊:Immunity
[Cell Press]
日期:2026-02-16
卷期号:59 (3): 542-558.e8
被引量:2
标识
DOI:10.1016/j.immuni.2025.12.017
摘要
The non-canonical inflammasome, comprising caspase-4 in humans, initiates pyroptosis upon sensing cytosolic lipopolysaccharide (LPS) from Gram-negative bacteria. Caspase-4 activation also depends on several guanylate-binding proteins (GBPs), which associate with the surface of cytosolic bacteria. Here, we investigated how caspase-4 accesses its cognate ligand, the hydrophobic lipid A moiety of LPS, and the role of GBPs in this process. GBP1 was essential for caspase-4 activation during infection. Mechanistically, GBP1 deformed the LPS-containing outer membrane of cytosolic bacteria, acting as a GTP-dependent mechanoenzyme. In vitro, GBP1 fragmented LPS micelles and promoted caspase-4/LPS complex formation, thereby enhancing LPS-induced caspase-4 activation. Fragmented LPS micelles presented additional micelle tips that served as binding and activation sites for caspase-4, indicating that caspase-4 engages LPS membranes with defined geometry rather than individual LPS molecules. Thus, GBP-mediated deformation of the LPS-rich outer bacterial membrane generates regions of positive curvature that expose lipid A, enabling caspase-4 binding, oligomerization, and activation.
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