ArticleCell reports2025
Global genome analysis identifies glycolipids and lipoteichoic acid alanylation as contributors to group B streptococcal diabetic wound infection.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- The diabetic wound microenvironment drives emergence and maintenance of CovRS variants in group BInfection and immunity · 2026Article
- Group B streptococcal membrane vesicles induce proinflammatory responses in neonatal meninges.Infection and immunity · 2026Article
- A murine model of adult gastrointestinal colonization by Group BInfection and immunity · 2026Article
- Enhancement of low-temperature growth ofbioRxiv : the preprint server for biology · 2026Article
- A murine model of adult gastrointestinal colonization by Group BbioRxiv : the preprint server for biology · 2025Article
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Abstract
Diabetic individuals frequently develop chronic, hyper-inflammatory, non-healing wounds, which are the leading cause of all non-traumatic amputations. Group B Streptococcus (GBS) is a prominent bacterium isolated from diabetic wound infections, and in a murine model of diabetic wound infection, GBS stimulates an influx of neutrophils into the wound. Utilizing a transposon mutant screen, we identified 291 bacterial genes required for fitness during diabetic wound infection, including enzymes involved in glycolipid biosynthesis and lipoteichoic acid (LTA) alanylation. GBS mutants lacking either LTA alanylation (ΔdltA) or all glycolipids (ΔiagB) are attenuated in murine diabetic wound infection. GBS induces primary and secondary degranulation in primary human neutrophils, and the ΔiagB mutant is significantly more susceptible to neutrophil killing by cationic antimicrobial peptides and reactive oxygen species than ΔdltA. Finally, we found that depletion of neutrophils led to significantly greater bacterial recovery, highlighting the importance of neutrophil defense during diabetic wound infection.
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