Coconnier M H, Dlissi E, Robard M, Laboisse C L, Gaillard J L, Servin A L
CJF 94.07 INSERM, Pathogénie Cellulaire et Moléculaire des Microorganismes Entérovirulents, Faculté de Pharmacie Paris XI, F-92296 Châtenay-Malabry, France.
Infect Immun. 1998 Aug;66(8):3673-81. doi: 10.1128/IAI.66.8.3673-3681.1998.
When the intracellular pathogen Listeria monocytogenes infects cultured human mucosecreting polarized HT29-MTX cells apically, it induces the stimulation of mucus exocytosis without cell entry. Using a set of isogenic mutants and purified listeriolysin O (LLO), we identified the L. monocytogenes thiol-activated exotoxin LLO as the agonist of mucus secretion. We demonstrated that the LLO-induced mucus exocytosis did not result from the LLO membrane-damaging activity. We found that LLO-induced mucus exocytosis is an event requiring the binding of LLO to a brush border-associated receptor and membrane oligomerization of the exotoxin. By a pharmacological approach, we demonstrated that no regulatory system or intracellular transducing signal known to be involved in control of mucin exocytosis was activated by LLO. Based on the present data, the stimulatory action of LLO on mucin exocytosis could be accounted for either by an unknown signaling system which remains to be determined or by direct action of LLO with the membrane vesicle components involved in the intracellular vesicular transport of mucins.
当细胞内病原体单核细胞增生李斯特菌从顶端感染培养的人黏液分泌极化HT29-MTX细胞时,它会在不进入细胞的情况下诱导黏液胞吐作用的刺激。使用一组同基因突变体和纯化的李斯特菌溶血素O(LLO),我们确定单核细胞增生李斯特菌硫醇激活外毒素LLO为黏液分泌的激动剂。我们证明LLO诱导的黏液胞吐作用并非源于LLO的膜损伤活性。我们发现LLO诱导的黏液胞吐作用是一个需要LLO与刷状缘相关受体结合以及外毒素膜寡聚化的事件。通过药理学方法,我们证明LLO不会激活已知参与黏蛋白胞吐作用控制的任何调节系统或细胞内转导信号。基于目前的数据,LLO对黏蛋白胞吐作用的刺激作用可能是由一个有待确定的未知信号系统引起的,或者是由LLO与参与黏蛋白细胞内囊泡运输的膜囊泡成分直接作用导致的。