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OPSONIZATION OF GROUP B STREPTOCOCCI IN PROPERDIN DEFICIENT SERUM
Author(s) -
SöDERSTRöM C.,
BRACONIER J.H.,
CHRISTENSEN K.K.,
CHRISTENSEN P.,
SJöHOLM A.G.
Publication year - 1985
Publication title -
acta pathologica microbiologica scandinavica series c: immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0108-0202
DOI - 10.1111/j.1699-0463.1985.tb02953.x
Subject(s) - properdin , antibody opsonization , microbiology and biotechnology , group (periodic table) , group a , group b , medicine , immunology , chemistry , biology , opsonin , antibody , complement system , organic chemistry
Phagocytic killing of group B streptococci serotypes Ia, Ib, IIR‐ (R protein negative), IIR+ (R protein positive), IIIR‐ and IIIR+ by human granulocytes was studied after opsonization in properdin deficient serum, pooled normal human serum and in selected sera with high or low concentrations of antibody to group B streptococci. All serotypes were killed by granulocytes after opsonization in normal serum, but serotype IIIR‐ was comparatively resistant. Properdin deficient serum showed no opsonic activity for type IIIR‐. A reduced opsonic capacity of properdin deficient serum for serotypes Ib and IIR+ was demonstrated, whereas the other serotypes were efficiently opsonized. The reduced or absent opsonic activity of properdin deficient serum could be restored by addition of purified properdin. Antibody levels did not appear to be limiting in the assay system. Blocking of C1 activation with MgEGTA in normal serum delayed, but did not abolish opsonization of the various group B streptococcal serotypes, while the opsonic activity in chelated properdin deficient serum was markedly reduced. Taken together, the findings suggest that an intact classical pathway is crucial in group B streptococcal opsonization. However, efficient opsonization of some strains apparently requires that C3 activation on the bacterial surface is amplified through recruitment of the alternative pathway.