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Infect Immun. 1972 September; 6(3): 355-363
Copyright © 1972 American Society for Microbiology. All Rights Reserved.

Response of Mice to Injection of Ribosomal Fraction from Group B Neisseria meningitidis

David W. Thomas and Emilio Weiss

1 Department of Microbiology, Naval Medical Research Institute, Bethesda, Maryland 20014

ABSTRACT

Ribosomes of strain NOR-7 of group B Neisseria meningitidis were isolated by a procedure that included treatment of the cells with sodium dodecyl sulfate, disruption in a French pressure cell, and differential centrifugation. These preparations consisted of 66% ribonucleic acid and 24% protein and sedimented as a single component with a constant of approximately 66S. When used in immunodiffusion tests with homologous rabbit antiserum, untreated ribosomes formed two precipitin lines, when treated with ribonuclease three lines, and when Pronase-digested only one distinct line. Qualitatively indistinguishable reactions were obtained with the same antiserum and ribosomes from group A meningococci, but no precipitation occurred with those of Escherichia coli. When injected into mice, group B ribosomes elicited an increase in the number of antibody-producing spleen cells demonstrable by the hemolytic plaque technique using unsensitized sheep erythrocytes. Sensitization of the erythrocytes with increasing amounts of supernatant fluid of meningococcal cultures progressively reduced the number of demonstrable plaque-forming cells. Neuraminidase treatment of the erythrocytes increased immune hemolysis, whereas Pronase digestion reduced it. Injected mice were protected against homologous and heterologous meningococcal challenge. Both hemolysis and protection-inducing activities of the ribosomes were unimpaired by ribonuclease, but were reduced by Pronase. It is concluded that the immunological response elicited by the meningococcal ribosomes does not involve the group-specific carbohydrate antigen. The immunological mechanism by which the mice are protected against meningococcal challenge remains unknown.


Infect Immun. 1972 September; 6(3): 355-363
Copyright © 1972 American Society for Microbiology. All Rights Reserved.







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