Group B Streptococcus Induces a Caspase‐Dependent Apoptosis in Fetal Rat Lung Interstitium

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Group B Streptococcus (GBS) is an important fetal, neonatal, and infant pathogen. Using an ex vivo infection model, GBS induced profound reductions in fetal lung; explant size, airway branching, and erythroblast island areas. Elevated levels of apoptosis subsequent to GBS infections were observed by whole‐mount confocal immunofluorescence using activated‐caspase‐3‐antibodies and terminal deoxynucleotidyl transferase dUTP nick end‐labeling (TUNEL) assays. The caspase inhibitor Z‐VAD‐FMK abolished the increase in TUNEL‐positive cells associated with GBS infections, indicating that the GBS‐induced apoptosis was caspase‐dependent. Digital image analyses revealed that both GBS and the active form of caspase‐3 were distributed primarily within the lung interstitium, suggesting that these tissues are important targets for GBS. Antibodies to the active form of caspase‐3 colocalized with both macrophage‐and erythroblast‐markers, suggesting that these hematopoietic cells are GBS targets. These studies suggest that GBS infections profoundly alter lung morphology and that caspase‐dependent hematopoietic cell apoptosis within the lung interstitium.

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