Antibodies to lipopolysaccharide block adherence of shiga toxin-producing Escherichia coli to human intestinal epithelial (Henle 407) cells.

Abstract

Shiga toxin-producing Escherichia coli (STEC) are a diverse group of organisms known to cause diarrhoea, haemorrhagic colitis and haemolytic uraemic syndrome (HUS) in humans. During the early stage of infection, numbers of STEC in the gut may be very high (of the order of 10(9)/g faeces), but as disease progresses, the numbers may drop rapidly such that STEC are undetectable within a week. Convalescent sera from patients recovering from HUS frequently contain high levels of antibody to E. coli lipopolysaccharide (LPS) of the infecting serotype, and it is possible that a local immune response to LPS contributes to elimination of the organism from the gut. We have recently demonstrated that STEC strains isolated from HUS cases have enhanced adherence to a human intestinal epithelial cell line (Henle 407) compared with STEC strains from non-human sources. In this study, we examined the capacity of STEC strains belonging to O-antigen types O111 and O157 to adhere to human intestinal epithelial (Henle 407) cells in the presence or absence of anti-LPS. Adherence was inhibited by up to 95% by anti-LPS of the homologous, but not heterologous serotype. This effect was not an artefact of serum bactericidal or agglutinating activity. Preincubation with purified homologous or heterologous LPS did not prevent adherence, suggesting that LPS was not acting as an adhesin per se. Nevertheless, these findings raise the possibility that oral administration of preparations containing anti-LPS may interfere with colonization of the human gut by STEC, and therefore could be of potential therapeutic value if administered early in the course of infection.