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SLPI in UTI

ABSTRACT: Secretory Leukocyte Protease Inhibitor Protects Against Severe Urinary Tract Infection in Mice

PROVIDER: PRJEB66138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12051223_1.fastq.gz	Fastqsanger.gz
	ERR12051223_2.fastq.gz	Fastqsanger.gz
	ERR12051224_1.fastq.gz	Fastqsanger.gz
	ERR12051224_2.fastq.gz	Fastqsanger.gz
	ERR12051225_1.fastq.gz	Fastqsanger.gz

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Project description:Proteus mirabilis is a primary cause of complicated urinary tract infections (UTI). Surprisingly, iron acquisition systems have been poorly characterized in this uropathogen despite the urinary tract being iron-limited. In this report the transcriptome of strain HI4320, cultured under iron limitation, was examined using microarray analysis. Of genes upregulated at least 2-fold, 45 were statistically significant and comprise 21 putative iron-regulated systems. Two of these systems, PMI0229-0239 and PMI2596-2605, are organized in operons and appear to encode siderophore biosynthesis genes. Five microarrays comparing P. mirabilis HI4320 cultured in LB broth to P. mirabilis cultured in LB broth + 15 uM Desferal (an iron chelator) were analyzed. All five arrays are biological replicates; arrays #2 and 4 are dye swaps.

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Functional redundancy of iron acquisition systems is required for Proteus mirabilis pathogenesis during UTI

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Project description:Phage therapy against urinary tract infections

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Project description:We used the myoma model in conjunction with gene expression profiling with microarray data as an efficient tool for high throughput analysis and to screen for differentially expressed genes. Our aim was to identify candidates playing an important role in SLPI and/or MMP-promoted tumor invasion by comparing oral carcinoma Ca9-22 cells, which highly express secretory leukocyte protease inhibitor (SLPI) gene, with SLPI-deficient Ca9-22 cells. In oral carcinoma Ca9-22 and SLPI-deficient Ca9-22 (ÎSLPI) samples, gene expression profiling was performed with the Affymetrix Human Genome U133 Plus 2.0 Array. Two arrays for 2 cell lines were analyzed.

2016-08-22 | E-GEOD-78501 | biostudies-arrayexpress

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.

2021-11-01 | GSE186800 | GEO

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