دورية أكاديمية
Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota.
العنوان: | Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota. |
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المؤلفون: | Mercado-Evans V; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA.; Medical Scientist Training Program, Baylor College of Medicine, Houston, TX, 77030, USA., Mejia ME; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA., Zulk JJ; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA., Ottinger S; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA., Hameed ZA; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA., Serchejian C; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA., Marunde MG; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA., Robertson CM; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA., Ballard MB; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA., Ruano SH; Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX, 77030, USA., Korotkova N; Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, KY, USA.; Department of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY, USA., Flores AR; Division of Infectious Diseases, Department of Pediatrics, McGovern Medical School, UTHealth Houston, Children's Memorial Hermann Hospital, Houston, TX, USA., Pennington KA; Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX, 77030, USA., Patras KA; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA. katy.patras@bcm.edu.; Alkek Center for Metagenomics and Microbiome Research, Baylor College of Medicine, Houston, TX, 77030, USA. katy.patras@bcm.edu. |
المصدر: | Nature communications [Nat Commun] 2024 Feb 03; Vol. 15 (1), pp. 1035. Date of Electronic Publication: 2024 Feb 03. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: [London] : Nature Pub. Group |
مواضيع طبية MeSH: | Diabetes, Gestational* , Microbiota* , Streptococcal Infections*/microbiology, Pregnancy ; Female ; Humans ; Animals ; Mice ; Infectious Disease Transmission, Vertical ; Cytokines ; Vagina/microbiology ; Streptococcus ; Streptococcus agalactiae |
مستخلص: | 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. (© 2024. The Author(s).) |
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معلومات مُعتمدة: | R21 AI149366 United States AI NIAID NIH HHS; P30 CA125123 United States CA NCI NIH HHS; R25 GM056929 United States GM NIGMS NIH HHS; P30 DK056338 United States DK NIDDK NIH HHS; U19 AI157981 United States AI NIAID NIH HHS; S10 RR024574 United States RR NCRR NIH HHS; T32 GM152777 United States GM NIGMS NIH HHS; R21 AI173448 United States AI NIAID NIH HHS; T32 GM136554 United States GM NIGMS NIH HHS; R01 DK128053 United States DK NIDDK NIH HHS; F31 AI167547 United States AI NIAID NIH HHS; F31 HD111236 United States HD NICHD NIH HHS; F31 AI167538 United States AI NIAID NIH HHS |
المشرفين على المادة: | 0 (Cytokines) |
تواريخ الأحداث: | Date Created: 20240203 Date Completed: 20240205 Latest Revision: 20240611 |
رمز التحديث: | 20240611 |
مُعرف محوري في PubMed: | PMC10838280 |
DOI: | 10.1038/s41467-024-45336-6 |
PMID: | 38310089 |
قاعدة البيانات: | MEDLINE |
تدمد: | 2041-1723 |
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DOI: | 10.1038/s41467-024-45336-6 |