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The loss of contact inhibition and anchorage‐dependent growth are key steps in the acquisition of Listeria monocytogenes susceptibility phenotype by non‐phagocytic cells
Author(s) -
Velge Philippe,
Kaeffer Bertrand,
Bottreau Elisabeth,
Langendonck Nathalie
Publication year - 1995
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1111/j.1768-322x.1995.tb00942.x
Subject(s) - listeria monocytogenes , biology , intracellular , phenotype , transformation (genetics) , cell culture , cell , microbiology and biotechnology , contact inhibition , listeria , bacteria , genetics , gene
Summary— We have previously demonstrated that intestinal and kidney finite cell lines were resistant to L monocytogenes invasion ( ie allowed low bacterial entry and no intracellular multiplication) in contrast to the continuous cell lines which were susceptible to Listeria invasion ( ie allowed high bacterial entry and intracellular multiplication) (Velge et al (1994a) Med Microbial Immunol 183, 145). The aim of this study was to discover whether epigenetic or genetic cellular modifications could convert L monocytogenes resistant cells into a susceptible phenotype and to determine the cellular steps involved in Listeria susceptibility. Among the 5‐azacytidine treated finite cell lines, the untransformed immortal cell lines established remained resistant to L monocytogenes invasion whereas the weakly transformed continuous cell lines established were converted into a susceptible phenotype. Transfection of resistant cells by SV40 large T antigen induced only highly transformed continuous cell lines displaying a susceptible phenotype. Taken together these data show that cell transformation enhanced Listeria invasion. This conclusion was supported by the observation that L monocytogenes was able to induce cell foci within murine finite cell monolayers. This morphological cell transformation was completely reversible and required live bacteria inside cells. In conclusion, we may speculate that the L monocytogenes intracellular multiplication observed within cell foci could be explained by the loss of contact inhibition of the finite cell monolayer. Indeed, the loss of both contact inhibition and anchorage‐dependent growth are the key steps involved in the L monocytogenes susceptibility phenotype.