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The Journal of Medical Microbiology, Vol 26, Issue 1 29-35, Copyright © 1988 by Society for General Microbiology
JOURNAL ARTICLE |
P. Williams, P. A. Lambert and M. R. Brown
Department of Pharmaceutical Sciences, Aston University, Birmingham.
The ability of antibodies to cell-surface components of Klebsiella to increase surface hydrophobicity and to gain access to antigens potentially masked by the capsule was investigated. Treatment of capsulate or non-capsulate strains with the respective autologous antiserum resulted in a marked increase in surface hydrophobicity. Antisera raised against a rough non-capsulate (K-O-) strain had little effect on the surface hydrophobicity of either of the capsulate strains K1+O1+ and K2+O1+, or of the non-capsulate K-O1+ strain. Whereas anti-K-O1+ sera or anti-K2+ sera increased the surface hydrophobicity of the K2+O1+ strain, only antisera containing anti-K1+ antibodies increased the hydrophobicity of the K1+O1+ strain. Immunoadsorption of anti-K-O1+ serum by whole capsulate cells revealed that neither the K1 nor the K2 capsular polysaccharide acted as a barrier to anti-O antibodies but that the K1 capsular polysaccharide masked the presence of the immunoglobulin at the cell surface. The Klebsiella capsular polysaccharide does not appear to present a permeability barrier to immunoglobulins although failure to detect outer-membrane proteins in the immune complexes of either of the capsulate strains or of the K-O1+ strain suggests that the O antigen may prevent access of antibodies to these antigens.
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