Abstract
Evidence that Listeria monocytogenes enters Caco-2 cells through the apical surface is presented. Attachment of bacteria to host cells seems to induce modifications of microvilli which are either in direct contact with the bacterial surface or in close vicinity, resulting in the formation of lamellipodia involved in the cellular uptake of the bacteria. Such modifications are not induced by L. monocytogenes SLCC 53, which carries a deletion in the prfA gene, although attachment of this mutant to Caco-2 cells occurs. 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 ethylene glycol-bis(beta-aminoethyl ether)- N,N,N1,N1-tetraacetic acid (EGTA), which disrupts intercellular junctions, greatly reduced the uptake of Listeria cells. Attachment and invasion of L. monocytogenes was not accompanied by accumulation of filamentous actin around the entering bacterial cell.
MeSH Terms
Bacterial Adhesion
Bacterial Proteins/genetics
Calcium/physiology
Colon/microbiology,ultrastructure
Humans
Listeria monocytogenes/pathogenicity
Peptide Termination Factors
Trans-Activators/genetics
Tumor Cells, Cultured
Chemicals
Bacterial Proteins
Peptide Termination Factors
Trans-Activators
Calcium
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Karunasagar I
Lehrstuhl Mikrobiologie, Theodor-Boveri-Institut für Biowissenschaften, Würzburg, Germany.
Senghaas B
Krohne G
Goebel W
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