The abstract is read at the publisher; the summary is JClub's.
BspC from hypervirulent ST-17 Streptococcus agalactiae increases neonatal mouse mortality and raises GBS burdens in intestine, blood, spleen, and brain versus a ΔbspC mutant.
- Why it matters: Neonatal GI colonization precedes invasive GBS disease, but how ST-17 strains persist in the gut and disseminate is not fully defined.
- What they did: In a neonatal mouse model, wild-type versus ΔbspC GBS were compared for organ burdens; BspC-dependent adherence was tested on a 2D human infant organoid model and Caco-2 cells, including Candida coinfection.
- The result: Candida albicans enhanced BspC-dependent epithelial adherence and, during coinfection, increased intestinal GBS burden and brain dissemination in neonatal mice; human infant fecal microbiome datasets showed higher GBS abundance with Candida colonization.
The findingWhy it mattersWhat they didThe result
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