Cardioselective β-blocker Therapy Resolves Staphylococcus aureus Toxin-Induced Innate Immunoparalysis

During Staphylococcus aureus sepsis, the pore-forming -toxin (Hla) triggers lytic platelet death and provokes the release of catecholamines that modulate leukocyte effector function. The resulting surge in catecholaminergic action paralyzes host antimicrobial capacity by upregulating interleukin-10 (IL-10), profoundly suppressing the protective interferon (IFN) response to orchestrate innate immunoparalysis. Here, we deconvolute a multi-cellular regulatory pathway in the blood and highlight a pivotal immunological checkpoint, where pharmacological intervention with cardioselective {beta}-blockers uncouples the immunosuppressive cascade, restores host antimicrobial function, and significantly improves survival outcomes.