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The effects of capsular polysaccharide on the capacity of serum to support the killing of type 3 Streptococcus pneumoniae by human neutrophils
Author(s) -
Esposito ANTHONY L.,
Clark CAROLYN A.
Publication year - 1990
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1990.tb05001.x
Subject(s) - streptococcus pneumoniae , microbiology and biotechnology , phagocytosis , polyclonal antibodies , antibody , polysaccharide , serotype , blood serum , superoxide , ingestion , pneumococcal infections , chemistry , biology , immunology , antibiotics , biochemistry , endocrinology , enzyme
To assess the effects of purified capsular polysaccharide from type 3 S. pneumoniae (PPS‐3) on the capacity of serum to support pneumococcal killing by human neutrophils, varying concentrations of PPS‐3 (0.01–100 μg/ml) were incubated (4 °C) with pooled serum for 30 min, and the resulting preparation, termed absorbed serum, was evaluated in bactericidal and phagocytic assays. The ability of serum to promote the killing of type 3 S. pneumoniae was significantly reduced at 1.0 μg/ml PPS‐3; similarly, serum absorbed with 1.0 μg/ml PPS‐2 failed to support the killing of type 2 S. penumoniae. However, the impact of these penumococcal polysaccharides was serotype specific, since the killing of type 3 S. pneumoniae was not impaired in serum absorbed with PPS‐2, and the killing of type 2 S. pneumoniae was not attenuated in serum treated with PPS‐3. The failure of serum absorbed with PPS‐3 to promote the killing of type 3 S. pneumoniae was primarily a consequence of impaired bacterial ingestion; the reduction in phagocytosis was associated with parallel changes in superoxide anion release. The defects in phagocytosis and killing induced by PPS‐3 were not associated with alterations in classical or alternative complement pathway activity; however, they were highly correlated with changes in serum antibody levels to the polysaccharide. The addition of polyclonal human IgG to serum treated with PPS‐3 did not restore its capacity to support killing; however, preopsonization of the bacterium with the IgG preparation did partially correct the deficiency. Finally, neutrophils preincubated with serum containing 10.0 μg/ml PPS‐3 exhibited an impaired bactericidal activity against type 3 S. pneumoniae. Thus, these studies demonstrate that the presence of PPS‐3 decreases the capacity of serum to support the killing of type 3 S. pneumoniae by absorbing immunoglobulins and by generating factors that interfere with neutrophil function.