Group B streptococcal beta-hemolysin/cytolysin directly impairs cardiomyocyte viability and function

Area of Science:

• Cardiology
• Microbiology
• Toxicology

Background:

• Group B Streptococcus (GBS) is a primary cause of neonatal sepsis.
• Myocardial dysfunction significantly contributes to poor outcomes in neonatal sepsis.

Purpose of the Study:

• To investigate the impact of the GBS beta-hemolysin/cytolysin (Bh/c) exotoxin on cardiomyocyte viability, contractility, and calcium handling.
• To explore the potential of dipalmitoyl phosphatidylcholine (DPPC) in mitigating Bh/c-induced cardiac effects.

Main Methods:

• HL-1 cardiomyocytes and primary rat ventricular cardiomyocytes were exposed to wild-type GBS, a Bh/c mutant, or cell-free extracts.
• Cardiomyocyte viability, apoptosis, contractility, mitochondrial membrane potential, and calcium transients were assessed.
• The effects of the Bh/c inhibitor DPPC were evaluated.

Main Results:

• Exposure to GBS Bh/c significantly reduced cardiomyocyte contractility and viability, inducing necrosis and apoptosis.
• The GBS Bh/c toxin caused rapid loss of calcium transients and mitochondrial membrane depolarization.
• These detrimental effects were prevented by DPPC treatment.

Conclusions:

• GBS Bh/c rapidly induces cardiomyocyte dysfunction and death.
• DPPC effectively inhibits the cardiotoxic effects of GBS Bh/c.
• These findings suggest a therapeutic role for DPPC in managing cardiac dysfunction during neonatal GBS infections.