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.

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BibTeX RIS

BibTeX

@misc{sun2026cardioselective,
  title = {{Cardioselective β-blocker Therapy Resolves Staphylococcus aureus Toxin-Induced Innate Immunoparalysis}},
  author = {J. W. Sun and R. Siew and D. J. Gonzalez and B. Luna and S. Kanaji and G. Sakoulas},
  howpublished = {bioRxiv},
  year = {2026},
  month = oct,
  doi = {10.64898/2026.10.12.758599},
  url = {https://www.biorxiv.org/content/10.64898/2026.10.12.758599v1},
  note = {CC BY-NC-ND},
}

RIS

TY  - UNPB
TI  - Cardioselective β-blocker Therapy Resolves Staphylococcus aureus Toxin-Induced Innate Immunoparalysis
AU  - J. W. Sun
AU  - R. Siew
AU  - D. J. Gonzalez
AU  - B. Luna
AU  - S. Kanaji
AU  - G. Sakoulas
PY  - 2026
DA  - 2026/10/12
PB  - bioRxiv
DO  - 10.64898/2026.10.12.758599
UR  - https://www.biorxiv.org/content/10.64898/2026.10.12.758599v1
AB  - 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.
ER  -

Abstract

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