bioRxiv · 10.64898/2026.10.12.758599
Cardioselective β-blocker Therapy Resolves Staphylococcus aureus Toxin-Induced Innate Immunoparalysis
Abstract
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.
Explore related subjects
Keep this discovery
Explore connections, maps & timelines
Sun, J. W., Siew, R., Gonzalez, D. J., Luna, B., Kanaji, S., Sakoulas, G.. 2026-10-13. Cardioselective β-blocker Therapy Resolves Staphylococcus aureus Toxin-Induced Innate Immunoparalysis. https://doi.org/10.64898/2026.10.12.758599
Cite the original work for its findings. Save a collection to share your selection of sources.