In a way similar to the binding of blood cells after
demasking of their galactose residues, many, and often
pathogenic, bacteria attach to mucous endothelia via
lectins, for example, in the oro-gastro-intestinal tract,
after desialylation of the endothelial cells and exposure of the subterminal galactose residues (Kelm and Schauer, 1997). Such bacteria secrete sialidase which removes the protecting Sia moieties and can thus be considered as a spreading or virulence factor. Many efforts are presently undertaken to synthesize inhibitors of this glycosidase or soluble ligands that prevent adhesion.