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Complement activation and attack on autologous cell membranes induced by streptolysin-O
Infection and Immunity
|June 1, 1985
Summary
Streptolysin-O toxin binds to human antibodies, forming complexes that activate the complement system. This process damages host cells, potentially contributing to post-streptococcal disease.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Streptolysin-O toxin creates channels in mammalian cell membranes.
- The mechanism by which this toxin interacts with the host immune system is not fully understood.
Purpose of the Study:
- To investigate the interaction between Streptolysin-O and human serum antibodies.
- To determine the effect of this interaction on the complement system.
- To elucidate the role of this interaction in host tissue damage and disease pathogenesis.
Main Methods:
- Incubation of Streptolysin-O with human serum containing immunoglobulin G (IgG) antibodies.
- Measurement of complement component consumption (C4, C5, C3) and hemolytic activity.
- Analysis of terminal complement complex (C5b-9) formation on target cell membranes.
Main Results:
- Streptolysin-O binds to human IgG antibodies, forming immune complexes.
- These complexes potently activate the complement cascade, leading to rapid consumption of C4 and C5, and significant C3 conversion.
- Complement activation occurs on target cell membranes where Streptolysin-O polymers have bound, leading to the formation of C5b-9 complexes.
Conclusions:
- Streptolysin-O-antibody complexes act as foci for potent, antibody-dependent complement activation.
- This process leads to self-attack on host cells, perpetuating tissue damage.
- The findings suggest a role for this mechanism in the pathogenesis of post-streptococcal diseases and immune evasion by bacteria.