Infection of rabbit kidney cells (RK13) by enteropathogenic Escherichia coli as a model to study the dynamics of actin cytoskeleton.

Enteropathogenic Escherichia coli (EPEC) colonizes the intestinal mucosa and causes a cell lesion known as attachment and effacement (A/E) lesion. The molecular mechanisms for A/E lesions include injection of Tir, which is a receptor for an adhesin named intimin. The Tir-intimin interaction causes rearrangement of the cytoskeleton forming actin-rich structures called pedestals. Unfortunately, the formation of the A/E lesions and the dynamics of the actin cytoskeleton during this rearrangement induced by EPEC cannot be studied in the natural host. However, there are EPEC strains that infect rabbit (REPEC) that are genetically and pathologically similar to EPEC. Here, we used REPEC for the infection of rabbit kidney epithelial cells, line RK13, as a model to understand the actin cytoskeleton dynamics during pedestal formation. Actin-rich pedestal formation during the infection of RK13 cells by REPEC was analyzed by electron and confocal microscopy. The kinetics of infection along with the use of antibiotics for eliminating the bacteria, as well as reinfection, evidenced the plasticity of the actin cytoskeleton during pedestal formation. Thus, this model is a helpful tool for studying the dynamics of actin cytoskeleton and for correlating the data with those observed in in vivo models in rabbits experimentally infected with REPEC.