SERUM OPSONIC DEFICIENCY PRODUCED BY STREPTOCOCCUS-PNEUMONIAE AND BY CAPSULAR POLYSACCHARIDE ANTIGENS

  • 1 January 1978
    • journal article
    • research article
    • Vol. 51  (5) , 527-538
Abstract
The opsonic requirements for phagocytosis of S. pneumoniae types 6, 7, 18 and 23 were determined in normal and C2[complement component 2]-deficient sera, and in normal serum chelated with magnesium ethyleneglycotetraacetic acid. All 4 strains were effectively opsonized via the alternative C pathway, suggesting that the capsular polysaccharides [CPS] of these strains activated C via the alternative pathway. Since bacteremic pneumococcal disease is often associated with circulating CPS, this cellular component may activate C in vivo and impair host defenses by producing an opsonic defect for pneumococci. Serum was incubated with suspensions of whole S. pneumoniae types 6, 7, 18 or 23 or with purified CPS from each of these types and residual C activity and opsonic capacity were measured. C 3-9 hemolytic activity and opsonic capacity for 3H-thymidine labeled Salmonella typhimurium, a species effectively opsonized via the alternative pathway, were reduced in serum following incubation. PS concentrations as low as 1 .mu.g/ml inhibited serum opsonic capacity for Salmonella. Whole pneumococci and pneumococcal CPS inhibited the opsonic activity of human C2-deficient serum for Salmonella, providing further evidence for activation of C via the alternative pathway. Pneumococcal CPS markedly inhibited the opsonic capacity of normal serum for the homologous pneumococcal type. Amounts of pneumococcal CPS similar to those found in the serum of patients with pneumococcal disease bring about decomplementation of serum via activation of the alternative pathway and inhibit pneumococcal opsonization.