The absence of PspA or presence of antibody to PspA facilitates the complement-dependent phagocytosis of pneumococci in vitro.

Abstract

Pneumococcal surface protein A (PspA) is a surface molecule on pneumococci that is required for full virulence in mouse models of infection. PspA has been reported to inhibit complement deposition on the pneumococcal surface. It has been assumed that this decreased complement deposition results in the inefficient phagocytosis of wild-type pneumococci. However, an effect of PspA on phagocytosis had not been shown. Our present studies demonstrated that a loss of PspA by capsular type 3 strains WU2 and A66.1 led to enhanced complement-dependent phagocytosis of the pneumococci by the mouse macrophage cell line J774A.1. This observation was made using human complement as well as mouse complement. Since this enhanced phagocytosis could be blocked by antibody to complement receptor CR3 on J774A.1, it was concluded that PspA's effect on phagocytosis was due to its effect on the amount of deposited complement, which in turn helped opsonize the pneumococci for phagocytosis. Since these studies included new independent mutants lacking PspA, the results provide solid confirmation of the previously reported effects of PspA on pneumococcal virulence and complement deposition. Finally, we showed that antibody to PspA, which is also known to enhance complement deposition, also enhances the phagocytosis of pneumococci in a largely complement-dependent manner.

• Authors: Bing Ren, Jie Li, Kristopher Genschmer, Susan K Hollingshead, David E Briles
• Journal: Clinical and vaccine immunology : CVI (Clin Vaccine Immunol) Vol. 19 Issue 10 Pg. 1574-82 (Oct 2012) ISSN: 1556-679X [Electronic] United States
• PMID: 22855389 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)

Chemical References

• Antibodies, Bacterial
• Bacterial Proteins
• Opsonin Proteins
• pneumococcal surface protein A
• Complement System Proteins

Topics

• Animals
• Antibodies, Bacterial (immunology)
• Bacterial Proteins (genetics, immunology, physiology)
• Cell Line
• Complement Activation
• Complement System Proteins (immunology)
• Disease Models, Animal
• Female
• Macrophages (microbiology)
• Mice
• Mice, Inbred BALB C
• Mice, Inbred CBA
• Opsonin Proteins (genetics, immunology)
• Phagocytosis (immunology)
• Pneumococcal Infections (immunology)
• Streptococcus pneumoniae (immunology, pathogenicity)