Shigella Infection of Henle Intestinal Epithelial Cells: Role of the Host Cell

Abstract

The process of Henle 407 [human] embryonic intestinal epithelial cell infection by S. flexneri 2a M42-43 was studied in an in vitro model system. The role of the Henle cell was assessed. Entry of S. flexneri into cells was suppressed by reagents which inhibit uptake of particles by phagocytic cells. The compounds tested included cytochalasin B, dibutyryl-cyclic[c]AMP, choleragen (Vibrio cholerae enterotoxin), iodoacetate and dinitrophenol [DNP]. Cytochalasin B inhibited infection at concentrations of 1.0 .mu.g/ml or greater. Dibutyryl-cAMP at concentrations of 1 mM and choleragen at 0.1 .mu.g/ml caused significant suppression of infection. Iodoacetate or DNP at 0.1 mM concentrations inhibited internalization of virulent shigellae and a combination of these compounds inhibited infection at 0.01 mM concentrations. Pre-incubation of Henle cell monolayers with the combination of iodoacetate and DNP (0.05 mM) inhibited infection markedly. Infection of epithelial cells by S. flexneri in vitro is accomplished by an endocytic process induced by virulent bacteria. The process appears similar to uptake of particles by phagocytic cells. Ultrastructural analysis by transmission electron microscopy provided corroborative evidence of phagocytosis of shigellae by Henle cells. Intracellular bacteria were often observed within membrane-limiting vacuoles resembling phagosomes.