Listeria ivanovii is capable of cell-to-cell spread involving actin polymerization
Listeria ivanovii is capable of cell-to-cell spread involving actin polymerization
复制标题
伊万诺维李斯特菌能够通过肌动蛋白聚合进行细胞间传播
作者：
I. Karunasagar;Georg Krohne;Werner Goebel
李斯特菌被认为对动物具有致病性，但很少发现与人类感染有关。据称，L. ivanovii 缺乏 actA 基因，该基因在单增李斯特菌中编码与宿主细胞肌动蛋白相互作用所需的蛋白质。使用荧光显微镜和电子显微镜，我们证明L. ivanovii可以侵入哺乳动物细胞，裂解吞噬体膜，聚合宿主细胞肌动蛋白，重组肌动蛋白形成尾巴，并在细胞之间传播。然而，聚合酶链式反应无法检测到与actA基因同源的DNA。此外，L. ivanovii 缺乏在单核细胞增生李斯特菌中由 actA 编码的 90-kDa 表面蛋白。尽管能够在细胞间传播，但伊万诺利斯特氏菌与单增李斯特氏菌的显着差异在于无法在单层 3T3 成纤维细胞上形成斑块。
Listeria ivanovii has been considered to be pathogenic to animals but has rarely been found associated with human infections. It has been claimed that L. ivanovii lacks the actA gene, which in L. monocytogenes encodes a protein required for interaction with host cell actin. Using fluorescence microscopy and electron microscopy, we demonstrate that L. ivanovii can invade mammalian cells, lyse the phagosomal membrane, polymerize host cell actin, reorganize actin to form tails, and spread from cell to cell. However, no DNA homologous to the actA gene could be detected by polymerase chain reaction. Further, L. ivanovii lacks the 90-kDa surface protein which in L. monocytogenes is encoded by actA. Despite the ability to spread from cell to cell, L. ivanovii differed significantly from L. monocytogenes in being unable to form plaques on monolayers of 3T3 fibroblast cells.
DOI：
10.1073/pnas.87.16.6068
发表时间：
1990-08-01
影响因子：
11.1
作者：
DABIRI, GA;SANGER, JM;SOUTHWICK, FS
通讯作者：
SOUTHWICK, FS