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 and Kathryn A. Patras ()
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Vicki Mercado-Evans: Baylor College of Medicine
Marlyd E. Mejia: Baylor College of Medicine
Jacob J. Zulk: Baylor College of Medicine
Samantha Ottinger: Baylor College of Medicine
Zainab A. Hameed: Baylor College of Medicine
Camille Serchejian: Baylor College of Medicine
Madelynn G. Marunde: Baylor College of Medicine
Clare M. Robertson: Baylor College of Medicine
Mallory B. Ballard: Baylor College of Medicine
Simone H. Ruano: Baylor College of Medicine
Natalia Korotkova: University of Kentucky
Anthony R. Flores: Children’s Memorial Hermann Hospital
Kathleen A. Pennington: Baylor College of Medicine
Kathryn A. Patras: Baylor College of Medicine

Nature Communications, 2024, vol. 15, issue 1, 1-20

Abstract: 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.

Date: 2024
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DOI: 10.1038/s41467-024-45336-6

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