Cervicovaginal Microbial-Immune State and Group B Streptococcus Colonization in Pregnancy.
Journal
American journal of perinatology
ISSN: 1098-8785
Titre abrégé: Am J Perinatol
Pays: United States
ID NLM: 8405212
Informations de publication
Date de publication:
09 Aug 2023
09 Aug 2023
Historique:
medline:
10
8
2023
pubmed:
10
8
2023
entrez:
9
8
2023
Statut:
aheadofprint
Résumé
Maternal colonization with Group B This was a secondary analysis of a prospective cohort study of pregnant individuals with singleton pregnancies who had CV microbiota specimens analyzed at 16 to 20, 20 to 24, and 24 to 28 weeks' gestation, along with a third trimester GBS rectovaginal (RV) culture ( Of 492 individuals, 34.3% were GBS RV + . Compared with individuals with CST I at 16 to 20 weeks, individuals with CST IV-A and CST II had a significantly elevated relative risk of subsequent GBS RV+ status. When stratified by high and low β-defensin-2 levels, β-defensin-2 was found to be an effect modifier of the association between CST IV-A and GBS RV+ status. In individuals with low β-defensin-2 levels, CST VI-A was associated with GBS RV+ status, but among individuals with high β-defensin-2 levels, there was no such association (interaction Pregnant individuals with CV microbiota characterized by CST IV-A and CST II had significantly elevated risk of GBS RV colonization in the third trimester compared with those with CST I, and β-defensin-2 was an effect modifier of the association between CST IV-A and GBS RV+ status. Future research should investigate if manipulation of the CV microbiota can prevent GBS colonization, thereby reducing intrapartum antibiotic prophylaxis and the risks of neonatal GBS infection. · The relationship between the CV microbiota and GBS RV colonization is unknown.. · A Lactobacillus-deficient, anaerobic rich vaginal community, CST IV-A, is associated with increased risk of GBS RV colonization.. · β-defensin-2 is an effect modifier of the association between CST IV-A and GBS RV+ status..
Identifiants
pubmed: 37557898
doi: 10.1055/s-0043-1772226
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NINR NIH HHS
ID : R01 NR014784
Pays : United States
Informations de copyright
Thieme. All rights reserved.
Déclaration de conflit d'intérêts
None declared.