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Staphylococcal γ-Hemolysin AB and γ-Hemolysin CB Differentially Activate Murine Bone Marrow-Derived Mast Cells
Hikaru Inoue1, Haruka Sakakibara1, Shion Kamada1
1Department of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Abstract:
Staphylococcus aureus (S. aureus) produces various bicomponent pore-forming toxins (PFTs), including the γ-hemolysins (HlgAB and HlgCB) and leukocidins (LukAB and LukED). This study aimed to examine the effect of PFTs on murine bone marrow-derived mast cells (BMMCs). All the PFTs assessed in this study (HlgAB, HlgCB, LukAB, and LukED) were found to bind to BMMCs. Specifically, HlgAB and LukED, but not HlgCB or LukAB, induced membrane damage. Furthermore, only HlgAB induced BMMC degranulation, whereas HlgAB and HlgCB significantly augmented the degranulation caused by ionophore, immunocomplex, and staphylococcal δ-toxin. The augmentation of degranulation by HlgAB was impaired when a pore-formation defect mutant of HlgB (HlgBΔstem) was used. Conversely, the augmentation by HlgCB was unaffected following the use of HlgBΔstem, suggesting that HlgAB but not HlgCB augments degranulation in a pore-formation-dependent manner. These results highlight the novel roles for the staphylococcal γ-hemolysins HlgAB and HlgCB, as they differentially affect the degranulation of mast cells in the effector phase of allergic inflammation.
Insights
Staphylococcus aureus pore-forming toxins (PFTs) differentially impact mast cell degranulation. γ-hemolysins HlgAB and HlgCB modulate mast cell responses, influencing allergic inflammation.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Staphylococcus aureus produces pore-forming toxins (PFTs) like γ-hemolysins (HlgAB, HlgCB) and leukocidins (LukAB, LukED).
- Mast cells are key immune cells involved in allergic inflammation and defense against pathogens.
Purpose of the Study:
- To investigate the effects of S. aureus PFTs on murine bone marrow-derived mast cells (BMMCs).
- To elucidate the mechanisms by which HlgAB and HlgCB influence mast cell degranulation.
Main Methods:
- Binding assays to confirm PFT interaction with BMMCs.
- Assessment of membrane damage and degranulation responses.
- Utilizing pore-formation defective mutants (HlgBΔstem) to distinguish mechanisms.
Main Results:
- All tested PFTs (HlgAB, HlgCB, LukAB, LukED) bound to BMMCs.
- HlgAB and LukED induced direct membrane damage.
- HlgAB induced BMMC degranulation, while both HlgAB and HlgCB augmented degranulation induced by other stimuli.
- HlgAB-mediated augmentation was pore-formation dependent, unlike HlgCB.
Conclusions:
- Staphylococcal γ-hemolysins HlgAB and HlgCB play distinct roles in mast cell effector functions.
- These toxins differentially modulate mast cell degranulation, impacting allergic inflammation pathways.
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