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Interaction between human polymorphonuclear leukocytes and Streptococcus milleri group bacteria
Anna Wanahita1, Elizabeth A Goldsmith, Daniel M Musher
1Medical Service, Veterans Affairs Medical Center, Baylor College of Medicine, Houston, TX 77030, USA. wanahita@aol.com
Abstract:
Because Streptococcus milleri group (SMG) bacteria--Streptococcus constellatus, Streptococcus intermedius, and Streptococcus anginosus--exhibit a striking propensity to cause abscesses, the interaction of these organisms with human polymorphonuclear leukocytes (PMNL) was examined. After incubation in pooled normal human serum, SMG stimulated less chemotaxis than did Staphylococcus aureus, in contrast to viridans streptococci, which caused greater chemotaxis than did S. aureus. PMNL ingested greater numbers of SMG and viridans streptococci than S. aureus but killed these organisms more slowly and less completely. Relative resistance to killing by PMNL is expected in organisms that cause abscesses, and inhibition of chemotaxis may contribute to pathogenicity, because delayed arrival of PMNL gives a head start to proliferating bacteria. This study helps explain the capacity of SMG to cause abscesses. It is unclear, however, why viridans streptococci, bacteria that rarely produce abscesses, share some of these same properties.
Insights
Streptococcus milleri group (SMG) bacteria can cause abscesses by resisting killing by human immune cells (polymorphonuclear leukocytes, PMNL). SMG also inhibits PMNL arrival, aiding bacterial proliferation and infection.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Streptococcus milleri group (SMG) bacteria, including S. constellatus, S. intermedius, and S. anginosus, are known for causing abscesses.
- The interaction between SMG and human immune cells, specifically polymorphonuclear leukocytes (PMNL), is crucial for understanding their pathogenicity.
Purpose of the Study:
- To investigate the interaction of SMG with human PMNL.
- To elucidate the mechanisms by which SMG contribute to abscess formation.
Main Methods:
- Incubation of SMG with pooled normal human serum and PMNL.
- Assessment of PMNL chemotaxis, ingestion, and killing of SMG compared to Staphylococcus aureus and viridans streptococci.
Main Results:
- SMG stimulated less PMNL chemotaxis compared to Staphylococcus aureus.
- PMNL ingested higher numbers of SMG and viridans streptococci but exhibited slower and less effective killing.
- Viridans streptococci shared some resistance properties with SMG despite rarely causing abscesses.
Conclusions:
- Relative resistance to PMNL killing and inhibition of chemotaxis are key factors contributing to SMG's abscess-forming capacity.
- Further research is needed to explain why viridans streptococci share these properties without frequently causing abscesses.