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Gardnerella exposures alter bladder gene expression and augment uropathogenic Escherichia coli urinary tract infection in mice.

ABSTRACT: Gardnerella exposures alter bladder gene expression and augment uropathogenic Escherichia coli urinary tract infection in mice.

PROVIDER: PRJNA838982 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19243010.fastq.gz	Fastqsanger.gz
	SRR19243011.fastq.gz	Fastqsanger.gz
	SRR19243012.fastq.gz	Fastqsanger.gz
	SRR19243013.fastq.gz	Fastqsanger.gz
	SRR19243014.fastq.gz	Fastqsanger.gz

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Gardnerella exposures alter bladder gene expression and augment uropathogenic Escherichia coli urinary tract infection in mice.

Project description:The anaerobic actinobacterium Gardnerella was first isolated from the bladder by suprapubic aspiration more than fifty years ago. Since then, Gardnerella has been increasingly recognized as a common and often abundant member of the female urinary microbiome (urobiome). Some studies even suggest that the presence of Gardnerella is associated with urological disorders in women. We recently reported that inoculation of Gardnerella into the bladders of mice results in urothelial exfoliation. Here we performed whole bladder RNA-seq in our mouse model to identify additional host pathways involved in the response to Gardnerella bladder exposure. The transcriptional response to Gardnerella reflected the urothelial turnover that is a consequence of exfoliation, while also illustrating the activation pathways involved in inflammation and immunity. Additional timed exposure experiments in mice provided further evidence of a potentially clinically relevant consequence of bladder exposures to Gardnerella -- increased susceptibility to subsequent UTI caused by uropathogenic Escherichia coli. Together these data provide a broader picture of the bladder response to Gardnerella and lay the groundwork for future studies examining the impact of Gardnerella on bladder health.

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<i>Gardnerella</i> Exposures Alter Bladder Gene Expression and Augment Uropathogenic <i>Escherichia coli</i> Urinary Tract Infection in Mice.

Project description:The anaerobic actinobacterium Gardnerella was first isolated from the bladder by suprapubic aspiration more than 50 years ago. Since then, Gardnerella has been increasingly recognized as a common and often abundant member of the female urinary microbiome (urobiome). Some studies even suggest that the presence of Gardnerella is associated with urological disorders in women. We recently reported that inoculation of Gardnerella into the bladders of mice results in urothelial exfoliation. Here, we performed whole bladder RNA-seq in our mouse model to identify additional host pathways involved in the response to Gardnerella bladder exposure. The transcriptional response to Gardnerella reflected the urothelial turnover that is a consequence of exfoliation while also illustrating the activation of pathways involved in inflammation and immunity. Additional timed exposure experiments in mice provided further evidence of a potentially clinically relevant consequence of bladder exposure to Gardnerella-increased susceptibility to subsequent UTI caused by uropathogenic Escherichia coli. Together, these data provide a broader picture of the bladder's response to Gardnerella and lay the groundwork for future studies examining the impact of Gardnerella on bladder health.

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Gardnerella vaginalis activates host responses necessary for Escherichia coli recurrent UTI from bladder reservoirs

Project description:Recurrent urinary tract infections (rUTI) are a costly clinical problem affecting millions of women worldwide each year. The majority of rUTI cases are caused by uropathogenic Escherichia coli (UPEC). Data from humans and mouse models indicate that some instances of rUTI are caused by UPEC emerging from latent reservoirs in the bladder. Some studies have reported that women with vaginal dysbiosis, typically characterized by high levels of Gardnerella vaginalis and other anaerobes, are at increased risk of UTI. Multiple studies have detected G. vaginalis in urine collected by transurethral catheterization (to limit vaginal contamination), suggesting that some women experience routine urinary tract exposures. We recently reported that inoculation of G. vaginalis into the bladder triggers rUTI from UPEC bladder reservoirs in a mouse model. Here we performed whole bladder RNAseq to identify host pathways involved in G. vaginalis-induced rUTI. We identified multiple host pathways differentially expressed following G. vaginalis exposure. At the gene and transcript level, we identified upregulation of the orphan nuclear receptor Nur77 (aka Nr4a1) and Nur77-regulated genes. Pilot data from Nur77 knockout mice suggests that Nur77 is necessary for G. vaganalis exposure to trigger rUTI.

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Project description:Gardnerella sp. overview

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