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Group B Streptococcus (GBS) infection during pregnancy

ABSTRACT: Group B Streptococcus (GBS) infection during pregnancy

PROVIDER: PRJNA807379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18045305_1.fastq.gz	Fastqsanger.gz
	SRR18045305_2.fastq.gz	Fastqsanger.gz
	SRR18045306_1.fastq.gz	Fastqsanger.gz
	SRR18045306_2.fastq.gz	Fastqsanger.gz
	SRR18045307_1.fastq.gz	Fastqsanger.gz

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Group B Streptococcus (GBS) infection during pregnancy

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Gestational diabetes augments group B Streptococcus perinatal infection through disruptions in maternal immunity and the vaginal microbiota

Project description: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. We interrogated host-pathogen dynamics in a novel murine GDM model of GBS colonization and perinatal transmission. GDM mice had greater GBS in utero dissemination and subsequently worse neonatal outcomes. Dual-RNA sequencing revealed differential GBS adaptation to the GDM reproductive tract, including a putative glycosyltransferase (yfhO), and altered host responses. GDM disruption of immunity included reduced uterine natural killer cell activation, impaired recruitment to placentae, and altered vaginal cytokines. Lastly, we observed distinct vaginal microbial taxa associated with GDM status and GBS invasive disease status. Our translational model of GBS perinatal transmission in GDM hosts recapitulates several clinical aspects and enables discovery of host and bacterial drivers of GBS perinatal disease.

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Project description:Group B Streptococcus (GBS) is a pathobiont responsible for invasive infections in neonates and in the elderly. The transition from a commensal to an invasive pathogen relies on the timely regulation of a set of virulence factors. In this study, we characterized the role of the SaeRS two-component system in GBS pathogenesis. Loss-of-function mutations in the SaeR response regulator decrease virulence in mouse models of invasive infection . Transcriptome and in vivo analysis reveal a regulatory system specifically activated during infection to control the expression of only two virulence factors: the PbsP adhesin and the BvaP secreted protein. The in vivo surge in SaeRS-regulated genes is complemented by fine-tuning mediated by the repressor of virulence CovRS system to establish a coordinated response. Constitutive activation of the SaeRS regulatory pathway increases adhesion and invasion of epithelial and endothelial barriers, though at the cost of reduced virulence. In conclusion, SaeRS is a specialized and dynamic system that balances the invasion of host barriers with disease progression.

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