Identification of the major adherence ligand of Klebsiella pneumoniae in the receptor for coliphage T7 and alteration of Klebsiella adherence properties by lysogenic conversion

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Abstract
The adherence of laboratory and wild-type K. pneumoniae strains, isolated from sputum, urine and stool samples, to human buccal and intestinal and urinary tract epithelial cells was studied. Of 32 unencapsulated strains, 30 adhered to all epithelial cells tested. For K. pneumoniae strains lysogenic for AP3, a phage which causes conversion to resistance to coliphages T3, T7 and .vphi.I, were unable to adhere to epithelial cells. Of these strains, was cured from phage infection and became capable of adhering. Spontaneous mutants resistant to coliphage T7 and K. pneumoniae K59-sensitive cells preadsorbed with inactivated T7 particles did not adhere to epithelial cells. All strains capable of adhering were able to adsorb coliphage T7 and T3; all nonadhesive strains were not. AP3-like prophages were induced from 7 of 12 nonadhesive Klebsiella strains. A laboratory strain which was able to adhere was lysogenized with 2 of these phages. In both cases, the strain lost is ability to adsorb coliphages T3, T7 and .vphi.I and to adhere to human epithelial cells. All K. pneumonia adhesive strains agglutinated yeast cells; the nonadhesive strains did not. Competition studies showed that D-mannose and concanavalin A prevented adherence to human epithelial cells, yeast agglutination and adsorption of coliphage T7 to K. pneumonia cells. K. pneumoniae adherence to epithelial cells is mediated by the receptor for coliphages T7 (and T3), which in turn recognizes D-mannose in the receptors it binds.