Abstract
Cells isolated from a body are resistant to bacterial invasion but lose the resistance upon immortalization and transformation. In this work, interaction of immortalized 3T3 fibroblasts and their in vitro transformed analog 3T3-SV40 cells with opportunistic bacteria Serratia grimesii was studied in a conventional medium and after incubating the cells with an antioxidant N-acetylcysteine (NAC). The 3T3 cells were shown to be approximately twice less sensitive to S. grimesii infection than similar but virus-transformed 3T3- SV40 cells. Incubation of 3T3 cells with 10 and 20 mM NAC enhanced the invasion 1.6 and 2.5-fold, respectively. Under the same conditions, the invasion of 3T3-SV40 cells by the bacteria was enhanced 2.1 and 2.4- fold. These results show that 3T3 cells are more resistant to invasion by S. grimesii than 3T3-SV40 cells, and the difference is preserved after the cells are exposed to 10 and 20 mM NAC. Among the genes which expression is known to be increased by NAC, a special role plays E-cadherin shown to interact with surface proteins (invasins) of pathogenic bacteria. Incubation of 3T3 and 3T3-SV40 cells with NAC resulted in an increased expression of E-cadherin, which correlates with the increased sensitivity of these cells to invasion. Confocal fluorescence microscopy revealed, for the first time, colocalization of S. grimesii with E-cadherin of 3T3 and 3T3-SV40 cells indicating that E-cadherin can be involved in the penetration of S. grimesii into eukaryotic cells.
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