Why the study?
Fulminant myocarditis is a life-threatening inflammatory disease, but the mechanisms underlying its acute onset remain unknown.
Does anti-Cxcr2 treatment reduce mortality in a mouse model of fulminant viral myocarditis?
Population
Mouse model of fulminant myocarditis
Comparison
Blockade of the Cxcl2/Cxcl3-Cxcr2 axis vs control
Design
Preclinical animal and single-cell RNA-sequencing study
Key result
Early blockade of the Cxcr2 axis to prevent neutrophil self-recruitment reduced the mortality rate of mice with fulminant myocarditis from over 60% to 30% and improved cardiac function.
Authors
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Merits investigation for fulminant myocarditis; extends mouse data but leaves open human translation.
Does anti-Cxcr2 treatment reduce mortality in a mouse model of fulminant viral myocarditis?
Absolute Event Rate: 30% vs 60%
Cardiac-infiltrating neutrophils drive early cardiac dysfunction in fulminant viral myocarditis, and blocking the Cxcr2 axis significantly reduces mortality in a mouse model.
Li et al. (2023) studied Fulminant viral myocarditis. Cxcr2 blockade (SB225002) vs. PBS control was evaluated on Mortality rate. Early blockade of the Cxcr2 axis to prevent neutrophil self-recruitment reduced the mortality rate of mice with fulminant myocarditis from over 60% to 30% and improved cardiac function.