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Modulation of the adherence of group A streptococci to murine cells
Microbiologica
|July 1, 1987
Abstract:
The adherence of group A Streptococci to P388 cells increases after treatment with interferon-gamma; this enhancement is less when antifibronectin antibodies are used. In parallel, peritoneal murine elicited macrophages pretreated with fibronectin bind more bacteria. Moreover, two monoclonal antibodies obtained against group A Streptococci had different effects on the ability of microorganisms to adhere to phagocytic cells.
Insights
Interferon-gamma enhances group A Streptococcus adherence to cells, an effect reduced by antifibronectin antibodies. Fibronectin-coated macrophages also bind more bacteria, indicating its role in streptococcal infection.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Group A Streptococcus (GAS) is a significant human pathogen.
- Bacterial adherence to host cells is a critical step in infection.
- The role of fibronectin and immune modulators in GAS adherence requires further elucidation.
Purpose of the Study:
- To investigate the effect of interferon-gamma on GAS adherence to P388 cells.
- To determine the role of antifibronectin antibodies in modulating GAS adherence.
- To examine the influence of fibronectin on macrophage-bacterial interactions.
Main Methods:
- Treatment of P388 cells with interferon-gamma.
- Assessment of GAS adherence using antifibronectin antibodies.
- Pre-treatment of murine elicited macrophages with fibronectin.
- Evaluation of bacterial binding to fibronectin-treated macrophages.
- Analysis of the effects of monoclonal antibodies against GAS on adherence.
Main Results:
- Interferon-gamma significantly increased GAS adherence to P388 cells.
- Antifibronectin antibodies partially inhibited the interferon-gamma-induced enhancement of adherence.
- Macrophages pre-treated with fibronectin exhibited increased binding of GAS.
- Monoclonal antibodies against GAS demonstrated differential effects on bacterial adherence to phagocytic cells.
Conclusions:
- Interferon-gamma enhances GAS adherence, potentially via fibronectin-dependent mechanisms.
- Fibronectin plays a crucial role in mediating the interaction between GAS and phagocytic cells.
- Targeting fibronectin interactions may offer a therapeutic strategy against GAS infections.