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Group B Streptococcus induces apoptosis in macrophages
K Fettucciari1, E Rosati, L Scaringi
1Department of Clinical and Experimental Medicine, University of Perugia, Italy.
Journal of Immunology (Baltimore, Md. : 1950)
|October 18, 2000
Summary
Group B Streptococcus (GBS) induces apoptosis in macrophages, a key immune cell. This bacterial evasion strategy involves beta-hemolysin and calcium signaling, aiding GBS survival.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Group B Streptococcus (GBS) employs immune evasion strategies.
- Phagocytic killing is crucial for controlling bacterial infections.
- Understanding how GBS interacts with host immune cells is vital.
Purpose of the Study:
- To investigate if GBS induces apoptosis in murine macrophages.
- To elucidate the mechanisms underlying GBS-induced apoptosis.
Main Methods:
- GBS type III strain COH31 r/s used to treat murine macrophages.
- Apoptosis assessed via morphological changes and DNA fragmentation.
- Inhibition studies using cytochalasin D, EGTA, PMA, calphostin C, GF109203X, and protein synthesis inhibitors.
Main Results:
- GBS induces macrophage apoptosis, characterized by membrane permeability defects and DNA fragmentation.
- Apoptosis is independent of caspase-1/-3 but dependent on host protein synthesis.
- Calcium influx and protein kinase C activation are implicated in the apoptotic pathway.
- GBS beta-hemolysin appears crucial for inducing apoptosis, potentially via membrane damage and calcium influx.
Conclusions:
- GBS actively induces macrophage apoptosis as a novel immune evasion mechanism.
- The process involves GBS beta-hemolysin, calcium signaling, and protein kinase C.
- This bacterial strategy contributes to GBS pathogenesis by subverting host defenses.