Evaluation of the role of clathrin and bacterial viability in the endocytosis of .

is an obligate intracellular bacterium and causative agent of proliferative enteropathy. The pathogenesis of is not completely understood, including the endocytic mechanisms to access the host cell cytoplasm. In this study, we evaluated the mechanisms involved in endocytosis of using intestinal porcine epithelial cells (IPEC-J2). Confocal microscopy was used to co-localize and clathrin. Clathrin gene knockdown was then applied to verify whether endocytosis is clathrin-dependent. Finally, internalization of viable and non-viable (bacteria were inactivated by heat) organisms were assessed to study the role of the host cell during bacterial endocytosis. organisms were observed co-localized with clathrin by confocal microscopy but the amount of internalized in cells, with and without clathrin knockdown, did not differ statistically. The internalization of non-viable showed a decrease in the internalization in cells with less clathrin synthesis (P<0.05). The present study is the first to elucidate the involvement of clathrin in the endocytosis of . Clathrin-mediated endocytosis was shown to be an important, but not required, process for internalization in porcine intestinal epithelial cells. Independence of bacterial viability for host cell internalization was also confirmed.