Antibodies to Streptococci Pneumoniae in Sera and Secretions of Mothers and their Infants

  • Barry M. Gray
  • Rutherford B. PolhillJr.
  • David W. Reynolds
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 310)


Human milk normally contains antibodies against a variety of common pathogens, and there is epidemiologic evidence that breast-fed infants are less susceptible to certain gastrointestinal infections.1 The role of breastfeeding in protection against respiratory bacteria is less clear and is undoubtedly complicated by the practical and social factors that determine the exposure of infants to organisms such as the pneumococcus.2 The immunological mechanism of protection is assumed to be the presence of type-specific antibodies; however, there are no quantitative data on antibodies to pneumococci in human milk. In this paper we describe a prospective study of antibody levels to four common pneumococcal serotypes in mothers’ milk and in the sera and saliva of their infants during the first year of life. The pneumococcal types selected were types 6, 14, 19, and 23, which are the most common types associated with carriage and infection in early childhood.3 Because some of these capsular antigens bear structural similarities to oligosaccharides found in normal human secretions, we also studied the inhibitory effect of milk and saliva on the binding of type-specific antibodies to the pneumococcal polysaccharides.


Antibody Level Human Milk Inhibition ELISA Pneumococcal Carriage Capsular Antigen 
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  1. 1.
    A. S. Cunningham, J. Pediatr. 90: 726 (1977).PubMedCrossRefGoogle Scholar
  2. 2.
    P. Glezen, Adv. Exp. Biol. Med. (this symposium) (1991).Google Scholar
  3. 3.
    B. M. Gray and H. C. Dillon Jr., Pediatr. Infect. Dis. J. 5: 201 (1986).CrossRefGoogle Scholar
  4. 4.
    B. M. Gray, G. M. Converse, III, and H. C. Dillon Jr., J. Infect. Dis. 146: 923 (1980).CrossRefGoogle Scholar
  5. 5.
    B. M. Gray, J. Immunol. Methods 72: 269 (1979).CrossRefGoogle Scholar
  6. 6.
    B. M. Gray and H. C. Dillon Jr., J. Infect. Dis. 158: 948 (1988).PubMedCrossRefGoogle Scholar
  7. 7.
    B. M. Gray, M. L. Egan, and D. G. Pritchard, Pediatr. Res. 24: 68 (1988).Google Scholar
  8. 8.
    H. J. Killian, J. Mestecky, and M. W. Russell, Microbiol. Rev. 52: 296 (1988).Google Scholar
  9. 9.
    R. A. Insel, M. Amstey, and M. Pichichero, J. Infect. Dis. 152: 407 (1985).PubMedCrossRefGoogle Scholar
  10. 10.
    Y. Okamoto and P. L. Ogra, Acta Paediatr. Scand. (Suppl) 351: 137 (1989).CrossRefGoogle Scholar
  11. 11.
    L. Kenne and B. Lindberg, in: “The Polysaccharides,” G. O. Aspinall, ed., Vol. 2, p. 287, Academic Press, New York (1983).Google Scholar
  12. 12.
    E. A. Kabat and M. M. Mayer, in: “Experimental Immunochemistry,” E. A. Kabat and M. M. Mayer, eds., 2nd ed., p. 838, Charles C. Thomas, Springfield, IL (1961).Google Scholar
  13. 13.
    M. R. Wessels, V. Pozsgay, D. L. Kasper, and H. J. Jennings, J. Biol. Chem. 262: 8262 (1987).PubMedGoogle Scholar
  14. 14.
    R. Schneerson, J. B. Robbins, J. C. Parke Jr., C. Bell, J. J. Schlesselman, A. Sutton, Z. Wang, G. Schiffman, A. Karpas, and J. Shiloach, Infect. Immun. 52: 519 (1986).PubMedGoogle Scholar
  15. 15.
    R. L. Clancy, A. W. Cripps, A. J. Husband, and D. Buckley, Infect. Immun. 39: 491 (1983).PubMedGoogle Scholar
  16. 16.
    S. Strobel and A. Furguson, Food Addit. Contam. 3: 43 (1982).CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1991

Authors and Affiliations

  • Barry M. Gray
    • 1
  • Rutherford B. PolhillJr.
    • 1
  • David W. Reynolds
    • 1
  1. 1.Departments of Pediatrics and MicrobiologyUniversity of Alabama at BirminghamBirminghamUSA

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