This study tested whether recombinant *S. aureus* serine protease-like protein B (SplB) could sensitize mice and induce allergic airway inflammation (AAI), using repeated intratracheal inoculations of catalytically active vs. inactive SplB in wild-type and gene-deficient C57BL/6J mice (Rag2-/-, Il33-/-, F2rl1-/-).
Active SplB caused eosinophilic airway inflammation, hyperresponsiveness, mucus production, fibrosis, and specific serum IgE; this effect required both SplB proteolytic activity and a functional adaptive immune system. IL-33 (but not PAR2) was necessary for eosinophil tissue invasion.
Findings are from a murine model only — direct translation to human asthma is unproven. The study does not establish whether natural *S. aureus* airway colonization releases sufficient SplB concentrations to drive sensitization in humans. Only one S. aureus virulence factor was tested.
Clinicians should be aware that *S. aureus* colonization may not just be a consequence of asthma — SplB and similar bacterial proteases could actively drive allergic sensitization. This supports closer attention to *S. aureus* colonization status in patients with new or difficult-to-control asthma.
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