Listeria ivanovii is capable of cell-to-cell spread involving actin polymerization.

AUTOR(ES)

Karunasagar, I

RESUMO

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.

Documentos Relacionados

• Role of Listeriolysin O in Cell-to-Cell Spread of Listeria monocytogenes
• Intracellular and cell-to-cell spread of Listeria monocytogenes involves interaction with F-actin in the enterocytelike cell line Caco-2.
• Isolation of Listeria monocytogenes small-plaque mutants defective for intracellular growth and cell-to-cell spread.
• Entry of Listeria monocytogenes into Neurons Occurs by Cell-to-Cell Spread: an In Vitro Study
• Directed Egress of Animal Viruses Promotes Cell-to-Cell Spread