Vibrio parahaemolyticus thermostable direct hemolysin modulates cytoskeletal organization and calcium homeostasis in intestinal cultured cells
Vibrio parahaemolyticus thermostable direct hemolysin modulates cytoskeletal organization and calcium homeostasis in intestinal cultured cells
复制标题
DOI：
10.1128/iai.67.3.1139-1148.1999
复制
发表时间：
1999-03-01
影响因子：
3.1
通讯作者：
Fiorentini, C
中科院分区：
文献类型：
--
作者：
Fabbri, A;Falzano, L;Fiorentini, C
副溶血性弧菌是一种海洋细菌，是导致全球海鲜肠胃炎的主要原因。由该微生物分泌的46-kDa同源二聚体蛋白，即热稳定直接溶血素（TDH），被认为是参与细菌致病的主要毒力因子，因为高百分比的临床来源的菌株对TDH产生呈阳性。TDH是一种成孔毒素，其最广泛研究的作用是引起不同哺乳动物物种红细胞溶血的能力。此外，TDH在多种细胞中诱导主要由细胞变性组成的细胞毒性作用，这通常导致活力丧失。在这项工作中，我们研究了TDH诱导的IEC-6细胞（来自大鼠隐窝小肠），这是一个有用的细胞模型，用于研究肠细菌毒素的单层细胞的细胞变化。在允许细胞存活的实验条件下，TDM诱导细胞内钙的快速瞬时增加以及通过细胞周期的显著但可逆的进展速率降低。形态学的变化似乎是依赖于组织的微管网络，这似乎是优先的细胞骨架元素参与细胞反应的毒素。
Vibrio parahaemolyticus is a marine bacterium known to be the leading cause of seafood gastroenteritis worldwide. A 46-kDa homodimer protein secreted by this microorganism, the thermostable direct hemolysin (TDH), is considered a major virulence factor involved in bacterial pathogenesis since a high percentage of strains of clinical origin are positive for TDH production. TDH is a pore-forming toxin, and its most extensively studied effect is the ability to cause hemolysis of erythrocytes from different mammalian species. Moreover, TDH induces in a variety of cells cytotoxic effects consisting mainly of cell degeneration which often leads to loss of viability. In this work, we examined the cellular changes induced by TDH in monolayers of IEC-6 cells (derived from the rat crypt small intestine), which represent a useful cell model for studying toxins from enteric bacteria. In experimental conditions allowing cell survival, TDM induces a rapid transient increase in intracellular calcium as well as a significant though reversible decreased rate of progression through the cell cycle. The morphological changes seem to be dependent on the organization of the microtubular network, which appears to be the preferential cytoskeletal element involved in the cellular response to the toxin.