Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota
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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.
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Mining transcriptomic data for gestational diabetes mellitus: What public datasets reveal
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Group B Streptococcus Management During Pregnancy
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MMP8 Promotes NETosis in Gestational Diabetes Mellitus
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- Authors
- Mercado-Evans, V., Mejia, M. E., Zulk, J. J., Ottinger, S., Hameed, Z. A., Serchejian, C., Marunde, M. G., Robertson, C. M., Ballard, M. B., Ruano, S. H., Korotkova, N., Flores, A. R., Pennington, K. A., & Patras, K. A.
- Affiliations
- Baylor College of Medicine (US)
- University of Kentucky (US)
- Memorial Hermann (US)
- Corresponding author
- Patras, Kathryn A.
- ORCID
- Venue
- Nature Communications
- Published
- 2024-02-03
- Volume
- 15
- Issue
- 1
- Pages
- 1035-1035
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC10838280
- OpenAlex
- W4391509793
- Cited by
- 40
- References
- 154
- Citations by year
- 2026: 15 · 2025: 19 · 2024: 5 · 2023: 1
- FWCI
- 16.09
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons-TMC (Texas Medical Center) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (DK128053)
- U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (AI157981)
- U.S. Department of Health & Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development (AI173448)
- Burroughs Wellcome Fund (NGP10103)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Neonatal and Maternal Infections
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Life Sciences › Immunology and Microbiology › Microbiology › Reproductive tract infections research
- Keywords
- gestational diabetes mellitus, Streptococcus agalactiae, perinatal transmission, maternal immunity, vaginal microbiota, natural killer cells, placenta, neonatal diseases, bacterial adaptation to host, dysbiosis
- MeSH terms
- Animals, Female, Humans, Pregnancy, Streptococcal Infections, Streptococcus, Streptococcus agalactiae, Vagina, Cytokines, Diabetes, Gestational, Infectious Disease Transmission, Vertical, Mice, Microbiota
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