Shigella flexneri, a Gram negative bacillus, causes bacillary dysentery, an ulcerative disease of the human colon, by invading intestinal epithelial cells. Entry into epithelial cells occurs via an induced phagocytic process which involves the actino-myosin complex. The host-cell receptor and the transmembrane signal which initiate reorganization of the cytoskeleton are under study. Binding to integrins has recently been demonstrated in related models such as the entry of Yersinia pseudotuberculosis and Bordetella pertussis into cells. Bacterial genes necessary to achieve entry are located on five contiguous loci covering 30 kb on a 220 kb virulence plasmid in S. flexneri. Locus 2 has been particularly studied. Six genes organized as an operon encode highly immunogenic proteins among which IpaB (62 kD) and IpaC (48 kD) are the invasins of this microorganism which subsequently grows very rapidly within infected cells due to its capacity to lyse the membrane bound phagocytic vacuole. Once free within the cytoplasm, bacteria interact again with the cell cytoskeleton. They first express Olm (organelle like movement), a phenotype reflecting intracellular movement along actin stress cables. They subsequently express lcs (intracellular spread), a phenotype by which intracellular bacteria induce nucleation and polymerization of actin followed by accumulation of this material at one end of the bacillus. This process causes rapid random movement leading to the formation of protrusions which allow passage to adjacent cells. A combination of these two movements achieves bacterial colonization of the epithelium.