In vitro modulation of adherence and invasion ability of enteroinvasive escherichia coli by different viruses.

ABSTRACT

Studies on the relationship between viral and bacterial infections showed that in the context of viral infections the immunity of host organism is reduced temporarily, increasing the incidence of bacterial infections, like faster bacterial colonization of immunocompromised bodies, by increasing the level of expression of epithelial cell receptor for bacterial adesins. Modulation of viruses infected host cells signaling may also induce changes in the cytoscheleton, which may result in the increase / decrease invasion capacity of bacterial cells. Enteroinvasive Escherichia coli causes intestinal infections exploiting host cell function, which include the invasion into non-phagocytic eukaryotic cells such as epithelial and endothelial cells and associated host cell actin cytoskeletal rearrangements. One of our aims was to investigate the in vitro adherence and invasion capacity induced by an diarhhoeal enteroinvasive Escherichia coli strain in the presence of different viral strains Vaccinia virus (Poxviridae), measles virus (Paramyxoviridae II); echovirus 32 (Picornaviridae) and Herpes simplex virus 1 (Herpesviridae). The viral adsorption on HeLa cells was done for six hours at 370C, followed by the evaluation of bacterial adherence and invasion to HeLa cells performed by the adapted Cravioto’s method and gentamycin protection assay. Viral preinfection of the cellular substrate induced an increased bacterial adherence index, as well as changes in the adherence pattern from diffuse tu aggregative. In exchange, the general effect of viral infection on invasive bacterial capacity was the decrease of invasive ability. In conclusion, viral preinfection of the susceptible substrate influenced the adherence and invasion ability of enteroinvasive E. coli bacterial strain, as observed by the intensification of the adherence capacity, explaining the increased incidence of bacterial infections after viral infections, as well as faster bacterial colonization of immunocompromised hosts and by reducing the invasive capacity of epithelial cell by bacterial strains, pleading for increased incidence of extracellular pathogenic organisms in post-viral infections.