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Restricted deposition of C3 on M+ group A streptococci: correlation with resistance to phagocytosis
Abstract:
In this report, the mechanism of resistance to phagocytosis by group A streptococci and the participation of M protein in this process were studied. A quantitative fluorometric immunoassay was used to determine the amount of the opsonic third component of complement, C3, fixed by group A streptococci in the presence and absence of M protein. In the absence of M protein, phagocytosis was found to be dependent on the amount of C3 fixed. However, when M protein was present, the streptococci still bound sufficient C3 to have promoted phagocytosis, yet none was observed. Further investigation using immunofluorescent microscopy demonstrated that the C3 fixed to M+ chains was confined to dense patches, interspaced by areas devoid of detectable C3. This uneven distribution of C3 was dependent on the presence of a trypsin-sensitive structure; most likely the M protein. The significance of this restricted C3 deposition with respect to resistance to phagocytosis by group A streptococci is discussed.
Insights
Group A streptococci resist phagocytosis by unevenly distributing complement C3 on their surface via M protein. This prevents opsonization, hindering immune cell engulfment and promoting bacterial survival.
Area of Science:
- Microbiology
- Immunology
- Bacterial Pathogenesis
Background:
- Group A Streptococcus (GAS) is a significant human pathogen.
- Phagocytosis is a key host defense mechanism against bacterial infections.
- M protein is a major virulence factor of GAS, mediating resistance to phagocytosis.
Purpose of the Study:
- To elucidate the mechanism by which M protein confers resistance to phagocytosis in GAS.
- To investigate the role of complement component C3 deposition in M protein-mediated resistance.
Main Methods:
- Quantitative fluorometric immunoassay to measure C3 deposition.
- Immunofluorescent microscopy to visualize C3 distribution on bacterial surface.
- Assessment of phagocytosis in the presence and absence of M protein.
Main Results:
- Phagocytosis of GAS is dependent on C3 deposition in the absence of M protein.
- GAS expressing M protein bound sufficient C3 for opsonization but resisted phagocytosis.
- M protein caused restricted, patchy C3 deposition on the bacterial surface.
- This uneven C3 distribution was dependent on a trypsin-sensitive structure, likely M protein.
Conclusions:
- M protein confers resistance to phagocytosis by disrupting normal C3 deposition patterns.
- Restricted C3 deposition mediated by M protein impairs opsonization and subsequent phagocytosis.
- Understanding this mechanism is crucial for developing strategies against GAS infections.