Staphylococcal γ‐Hemolysin <scp>AB</scp> and γ‐Hemolysin <scp>CB</scp> Differentially Activate Murine Bone Marrow‐Derived Mast Cells

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.