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Group A Streptococcus induces apoptosis in human epithelial cells
1Departments of Microbiology and Immunology, National Cheng Kung University Medical College, Tainan, Taiwan.
Infection and Immunity
|August 24, 1999
Summary
Group A Streptococcus (GAS) infection triggers epithelial cell apoptosis, a programmed cell death pathway. Internalization of GAS and the caspase pathway are crucial for this process, with SPE B enhancing cell death.
Area of Science:
- Microbiology
- Cell Biology
- Pathogenesis
Background:
- Group A Streptococcus (GAS) internalization by epithelial cells is implicated in invasive diseases.
- Understanding the cellular fate of infected epithelial cells is crucial for elucidating GAS pathogenesis.
Purpose of the Study:
- To investigate the mechanism of epithelial cell death following GAS infection.
- To determine the role of GAS internalization and specific virulence factors in inducing apoptosis.
Main Methods:
- Infection of A-549 and HEp-2 epithelial cell lines with GAS.
- Assessment of apoptosis using morphological changes, DNA fragmentation, and propidium iodide staining.
- Evaluation of the role of streptococcal pyrogenic exotoxin B (SPE B) using isogenic mutants.
- Inhibition studies with cytochalasin D and caspase inhibitors.
Main Results:
- GAS infection induced significant apoptosis in A-549 and HEp-2 cells, exceeding spontaneous rates.
- GAS internalization was necessary for inducing epithelial cell apoptosis.
- A GAS mutant deficient in SPE B showed reduced ability to induce cell death.
- Caspase inhibitors and cytochalasin D blocked GAS-induced apoptosis, implicating the caspase pathway and cytoskeleton.
Conclusions:
- GAS actively induces apoptosis in epithelial cells, requiring bacterial internalization.
- The caspase-dependent pathway plays a significant role in GAS-mediated epithelial cell death.
- Streptococcal pyrogenic exotoxin B contributes to the apoptotic process, enhancing cell death.