RodA Promotes Intestinal Colonization by Group B Streptococcus
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Background
Group B Streptococcus (GBS) intestinal colonization is critical for the pathogenesis of late-onset (LO) disease in infants. Using a murine model, we explore the role of rodA which encodes a peptidoglycan polymerase RodA, belonging to the Shape, Elongation, Division, and Sporulation (SEDS) family, that participates in peptidoglycan synthesis and maintenance of cell wall integrity.
Methods
We investigated the contribution of rodA to GBS GI colonization, using a wild-type strain (A909 WT) and an isogenic in-frame deletion mutant of rodA (A909Δ rodA ). Morphological differences between the two strains were examined by microscopy and imaging studies, and the contribution of rodA to GI colonization was assessed in a murine model through monocolonization and cocolonization experiments. We evaluated the growth of the mutant strain under intestinal physiological stress conditions and characterized its interactions with host epithelial cells.
Results
A909Δ rodA showed a unique chaining/aggregation phenotype compared to the WT strain, with the presence of capsule maintained on TEM and colony immunoblotting. In murine cocolonization experiments, A909 WT outcompeted A909Δ rodA ; however, monocolonization experiments exhibited comparable colonization and bacterial burden across the GI tract. In vitro experiments revealed impaired growth in bile and an increase in adhesion to intestinal epithelial cells by the Δ rodA mutant.
Conclusion(s)
rodA has a role in GBS intestinal colonization. Deletion of rodA increases sensitivity to gastrointestinal stressors in vitro and causes a pronounced defect in competition in vivo, revealing a role for cell wall polymerase in gut fitness.
