By R. Doyle, I. Ofek
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Extra resources for Adhesion of Microbial Pathogens [no cover, index]
21'23'29'3° Comments and Conclusions We have described the methods of studying the hemagglutinins of E. coli bacteria. Similar methods have been used for studying hemagglutinins of other bacteria. It has to be mentioned, however, that when RBCs are used as target cells for studying bacterial adhesins, one must realize the 25I. Ofek and R. J. Doyle, in "Bacterial Adhesion to Cells and Tissues," p. 92. Chapman & Hall, New York, 1994. 26B. Nowicki, A. Labigne, S. Moseley, R. Hull, S. Hull, and J. Moulds, Infect.
22 used monoclonal antibodies (MAbs) for inhibition of H A caused by S fimbriae of E. coli and fimbrial components. The authors demonstrated that H A is caused by whole fimbriae and by the isolated adhesin component, but not by fimbriae lacking the adhesin. The MAbs against the functional adhesin protein, but not those against structural fimbrial component, inhibited the agglutination. The capacity of adhesin-specific MAbs to inhibit H A caused by the 17 S. M. Ip, P. B. Crichton, D. C. Old, and J.
S K. Jann and H. Hoschiitzky, Curr. Top. Microbiol. lmmunol. 151, 55 (1991). 9. D. G. Evans, D. J. , S. Clegg, and J. A. Panley, Infect. Immun. 25, 738 J0 I. E. Salit and E. C. Gotschlich, J. Exp. Med. 146, 1169 (1977). 11 T. K. Korhonen, V. Vaisanen, H. Saxen, H. Hultberg, and S. B. Svenson, Infect. 37, 286 (1982). 12 j. p. Duguid, S. Clegg, and M. I. Wilson, J. Med. Microbiol. 12, 213 (1979). 13 I. Orskov, A. Birch-Andersen, J. P. Duguid, J. Stenderup, and F. Orskov, Infect. 47, 191 (1985). Immun.