Capsular type-specific polysaccharide partially inhibits group B Streptococcus-induced pulmonary hypertension

Area of Science:

• Microbiology
• Immunology
• Pathophysiology

Background:

• Group B Streptococcus (GBS) sepsis is a significant neonatal health concern.
• The role of capsular type-specific polysaccharide in GBS pathogenesis and associated hemodynamic responses is not fully understood.

Purpose of the Study:

• To investigate the impact of varying capsular type-specific polysaccharide expression on GBS-induced hemodynamic changes in infant piglets.
• To elucidate the mechanisms underlying GBS-mediated pulmonary hypertension.

Main Methods:

• Infusion of GBS Type lb strains with different capsule amounts into anesthetized and unanesthetized infant piglets.
• Measurement of hemodynamic parameters including mean pulmonary artery pressure, pulmonary vascular resistance index, and cardiac index.
• Quantification of arterial plasma thromboxane B2 levels and assessment of dazmegrel's effect.

Main Results:

• GBS strains with smaller capsules or deficient in capsules induced significant pulmonary hypertension and reduced cardiac index.
• The GBS strain with a larger capsule exhibited moderate pulmonary hypertension, less severe than the other strains.
• The capsule-deficient GBS mutant caused greater pulmonary hypertension and higher thromboxane B2 levels compared to the large-capsule strain.
• Dazmegrel, a thromboxane A2 synthase inhibitor, reversed the pulmonary hypertension induced by both strains.

Conclusions:

• Capsular type-specific polysaccharide is not essential for acute hemodynamic responses in GBS sepsis.
• High expression of capsular polysaccharide on GBS surface partially inhibits GBS-induced pulmonary hypertension.
• This inhibition is mediated by reduced thromboxane A2 release.