Asset Details
Do you wish to reserve the book?
Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota
Do you wish to request the book?
Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota
2024
Overview
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.
Here, Marcado-Evans et al show that gestational diabetes enhances group B Streptococcus infection through altering host-microbe dynamics, disrupting maternal immunity, and perturbing the vaginal microbiota in a murine pregnancy model.
