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

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

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

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.

Original languageEnglish
JournalNature Communications
Volume15
Issue number1
DOIs
StatePublished - Dec 2024

Bibliographical note

Publisher Copyright:
© The Author(s) 2024.

ASJC Scopus subject areas

  • General Chemistry
  • General Biochemistry, Genetics and Molecular Biology
  • General Physics and Astronomy

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