Saka Héctor A, Gutiérrez Maximiliano G, Bocco José L, Colombo María I
Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología (CONICET), Universidad Nacional de Córdoba, Córdoba, Argentina.
Autophagy. 2007 Jul-Aug;3(4):363-5. doi: 10.4161/auto.4159. Epub 2007 Jul 19.
Vibrio cholerae is the causative agent of cholera in humans. In addition to the criticalvirulence factors cholera toxin and toxin coregulated pilus, V. cholerae secretes V.cholerae cytolysin (VCC), a pore-forming exotoxin able to induce cell lysis and extensivevacuolation. We have shown that this vacuolation is related to the activation of autophagyin response to VCC action. Furthermore, we found that the autophagic pathway wasrequired to protect cells upon VCC intoxication. Based on additional data presented here,we propose a model aimed to explain the mechanism of cell protection. We postulatethat VCC-induced autophagic vacuoles, which display features of multivesicular bodies and enclose the toxin, are implicated in cell defense through VCC degradation involvingfusion with lysosomes.
霍乱弧菌是人类霍乱的病原体。除了关键的毒力因子霍乱毒素和毒素共调节菌毛外,霍乱弧菌还分泌霍乱弧菌溶细胞素(VCC),这是一种能够诱导细胞裂解和广泛空泡化的成孔外毒素。我们已经表明,这种空泡化与自噬的激活有关,以响应VCC的作用。此外,我们发现自噬途径是细胞在VCC中毒时保护细胞所必需的。基于此处提供的其他数据,我们提出了一个旨在解释细胞保护机制的模型。我们推测,VCC诱导的自噬空泡具有多囊泡体的特征并包裹毒素,通过与溶酶体融合参与VCC降解,从而参与细胞防御。