Granulocyte phagocytosis of Streptococcus pneumoniae in properdin-deficient serum

Abstract

Properdin (P)-deficient human serum containing type-specific anticapsular antibodies and having an intact classical pathway of complement did not support efficient granulocyte phagocytosis of Streptococcus pneumoniae serotypes 6A, 14, 19F, 23F, or 35 in an opsonophagocytic assay. Compared with pooled control serum, the difference was most pronounced for serotypes 14 and 23F and at a final serum concentration of 16%. The reduced phagocytic killing of S. pneumoniae serotype 23F in P-deficient serum was due rather to defective opsonization than to impaired intracellular killing. The uptake of C3 by the serotype 23F strain was found to be low in P-deficient serum. The addition of native P promoted C3 fixation as well as opsonization. The activity of P was abolished by heat treatment (56°C, 30 min). Experiments with Mg EGTA to block Cl activation suggested that serotype 23F pneumococci were more dependent on the classical pathway for opsonization than were serotype 35 pneumococci, which appear to be partly opsonized through the alternative pathway alone.

Granulocyte functions and Neisseria meningitidis: influence of properdin‐deficient serum

“…Inherited deficiency or dysfunction of properdin predisposes t o meningococcal disease (2,15,(18)(19)(20). Several C3-dependent functions are impaired in properdin-deficient sera (1,2,18,(22)(23)(24).…”