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…
We haven't written up this one. bioRxiv has the full story — the link below goes straight to it.
