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The Journal of Immunology, 1965, 95: 131-140.
Copyright © 1965 by The American Association of Immunologists, Inc.

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Natural Resistance of Germ-Free Mice and Colostrum-Deprived Piglets to Group A Streptococci1

Gene H. Stollerman, Richard D. Ekstedt and Irun R. Cohen2

From the Samuel J. Sackett Research Laboratory, Department of Medicine, and the Department of Microbiology, Northwestern University Medical School, Chicago, Illinois

Abstract

A study was made of the resistance of germfree and conventional mice to direct challenge with Group A streptococci of graded virulence. Germ-free and conventional mice were highly, and equally, resistant to nonencapsulated strains of Group A streptococci lacking M protein. Greater susceptibility of germ-free mice could be demonstrated only with Group A strains containing both M protein and capsules. This difference could be abolished by a globulin fraction of normal mouse serum but not by normal mouse {gamma}-globulin or by homologous type-specific antiserum.

In vitro studies with bloods of germ-free mice and colostrum-deprived piglets provided additional evidence that phagocytosis of avirulent Group A streptococci required little, if any, specific antibodies. Bloods from these animals phagocytized and destroyed streptococci as readily as did their conventional counterparts. Thermolabile opsonins against avirulent Group A streptococci were readily demonstrable in the blood of colostrum-deprived piglets, whose serum contains only minute amounts of {gamma}-globulin. Absorption of the sera of these animals at low temperatures with large amounts of homologous streptococci resulted in some decrease in opsonization, but considerable residual phagocytosis was apparent. The leukocytes of colostrum-deprived, and of colostrum-fed, animals were equally capable of phagocytizing and destroying Group A streptococci in the presence or absence of specific opsonins.

Footnotes

1 Presented in part to the American Society for Clinical Investigation, April 29, 1963 (1).

This study was conducted under the sponsorship of the Commission on Streptococcal and Staphylococcal Diseases, Armed Forces Epidemiological Board, and was supported in part by the office of the Surgeon General, Department of the Army, and by Public Health Service Grant HE-02623 and A1-02844.

2 Dr. Cohen participated in this study during the tenure of a predoctoral traineeship from Public Health Service Grant 2 T1 A1 57.







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