Showing papers by "Arthur C. Ouwehand published in 1996"
TL;DR: It could be concluded that the adhesion inhibitor affects K88 and S-fimbriae and can be produced by LAB of enteric origin and proposed blocking of receptors by steric hindrance as the most likely mechanism.
Abstract: The aim of this study was to establish the specificity of the adhesion inhibitor produced by Lactobacillus spp in an in vitro adhesion assay The effect on the adhesion of enteropathogenic Escherichia coli expressing K88, CFA/I, CFA/II, CFA/IV and S-fimbriae by spent culture fluids from a number of lactic acid bacteria (LAB), from human and porcine enteric origin and non-enteric non-LAB were tested It was found that the adhesion of E coli 1107 (K88ac) was inhibited by spent culture fluids from several LAB of porcine and by one of the LAB of human enteric origin Spent culture fluid from L fermentum 104r inhibited adhesion of E coli strains with all K88 serotypes Adhesion mediated by fimbriae other than K88 was inhibited to little or no extent Adhesion of E coli cells expressing CFA/I, II or IV was poor CFA/II mediated adhesion and adhesion of S-fimbriated E coli was inhibited by LAB from both human and porcine enteric origin It could be concluded that the adhesion inhibitor affects K88 and S-fimbriae and can be produced by LAB of enteric origin We propose blocking of receptors by steric hindrance as the most likely mechanism Keywords: adhesion inhibition, E coli , ETEC, Lactobacillus spp, fimbriae
11 citations