Details

Autor(en) / Beteiligte

• Mercado-Evans, Vicki
• Mejia, Marlyd E.
• Zulk, Jacob J.
• Ottinger, Samantha
• Hameed, Zainab A.
• Serchejian, Camille
• Marunde, Madelynn G.
• Robertson, Clare M.
• Ballard, Mallory B.
• Ruano, Simone H.
• Korotkova, Natalia
• Flores, Anthony R.
• Pennington, Kathleen A.
• Patras, Kathryn A.

Titel

Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota

Ist Teil von

• Nature communications, 2024-02, Vol.15 (1), p.1035-20, Article 1035

Ort / Verlag

London: Nature Publishing Group UK

Erscheinungsjahr

2024

Quelle

MEDLINE

Beschreibungen/Notizen

• Group B Streptococcus (GBS) is a pervasive perinatal pathogen, yet factors driving GBS dissemination in utero are poorly defined. Gestational diabetes mellitus (GDM), a complication marked by dysregulated immunity and maternal microbial dysbiosis, increases risk for GBS perinatal disease. Using a murine GDM model of GBS colonization and perinatal transmission, we find that GDM mice display greater GBS in utero dissemination and subsequently worse neonatal outcomes. Dual-RNA sequencing reveals differential GBS adaptation to the GDM reproductive tract, including a putative glycosyltransferase ( yfhO ), and altered host responses. GDM immune disruptions include reduced uterine natural killer cell activation, impaired recruitment to placentae, and altered maternofetal cytokines. Lastly, we observe distinct vaginal microbial taxa associated with GDM status and GBS invasive disease status. Here, we show a model of GBS dissemination in GDM hosts that recapitulates several clinical aspects and identifies multiple host and bacterial drivers of GBS perinatal disease. Here, Marcado-Evans et al show that gestational diabetes enhances group B Streptococcus infection through altering host-microbe dynamics, disrupting maternal immunity, and perturbing the vaginal microbiota in a murine pregnancy model.