I. Karunasagar et al., ULTRASTRUCTURAL-STUDY OF LISTERIA-MONOCYTOGENES ENTRY INTO CULTURED HUMAN COLONIC EPITHELIAL-CELLS, Infection and immunity, 62(8), 1994, pp. 3554-3558
Evidence that Listeria monocytogenes enters Caco-2 cells through the a
pical surface is presented. Attachment of bacteria to host cells seems
to induce modifications of microvilli which are either in direct cont
act with the bacterial surface or in close vicinity, resulting in the
formation of lamellipodia involved in the cellular uptake of the bacte
ria. Such modifications are not induced by L. monocytogenes SLCC 53, w
hich carries a deletion in the prfA gene, although attachment of this
mutant to Caco-2 cells of curs. Listeria innocua does not attach well
to Caco-2 cells and also fails to cause structural alterations of the
microvilli. Treatment of confluent monolayers of Caco-2 cells with eth
ylene glycol-bis(beta-aminoethyl ether)-N,N,N'N'-tetraacetic acid (EGT
A), which disrupts intercellular junctions, greatly reduced the uptake
of listeria cells. Attachment and invasion of L. monocytogenes was no
t accompanied by accumulation of filamentous actin around the entering
bacterial cell.