Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| GSE174783_Norm.csv.gz | Csv | |||
| GSE174783_Raw.csv.gz | Csv |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
Project description:The impact of IL-33 on urinary tract infections (UTI) was assessed by comparing Il33KO mice with wild-type (WT) mice within the bladder;The effect of ILC2 on UTI was assessed by comparing Il5cre+/DTA+ mice with WT mice within the bladder.
2024-10-20 | GSE259362 | GEO
Project description:Role of ILC in bladder infection
| PRJNA731515 | ENA
Project description:Urinary tract infections (UTIs) are the most common bacterial infections in women. During UTI, the host mounts a rapid immune response to clear the invading pathogen from the bladder. Mast cells are tissue resident immune cells that are found in the bladder lamina propria and can serve as first responders to bacterial infections. Here, we investigated the role of the mouse mast cell receptor Mrgprb2 and its human homologue MRGPRX2 in UTI. During acute UTI, Mrgprb2 is activated by the antimicrobial peptide cathelicidin and mediates mast cell degranulation. Using Mrgprb2 knockout mice, we demonstrated that Mrgprb2 promotes immune cell recruitment and amplifies inflammation, leading to epithelial damage and increased bacterial burden. Pharmacological inhibition of Mrgprb2 with its antagonist osthole improved infection outcomes. Using a humanized MRGPRX2 knock-in mouse in which Mrgprb2 is replaced by human MRGPRX2, we show conserved function of the mouse and human receptors in the bladder. Our findings identify human mast cell receptor MRGPRX2 as a potential therapeutic target to improve patient outcomes during UTI.
2026-04-10 | GSE324031 | GEO
Project description:Urinary tract infections (UTI) are common and recurrent. Both host genetics and UTI history impact susceptibility to recurrent UTI (rUTI) in women and in animal models. To identify shared patterns of host response that correlate with susceptibility, we investigated bladder inflammatory and transcriptional kinetics in acute and rUTI models. We found that TNFɑ signaling kinetics differed with mouse strain and infection history. Mice resistant to severe UTI/rUTI displayed a robust TNFɑ-dependent inflammation during the first 6 hours of acute cystitis, which waned by 24 hours; mice that are susceptible varied in their early responses but were prone to severe inflammation at 24 hours post-infection. Depletion of TNFɑ in an rUTI model revealed that early TNFɑ signaling promoted colonization resistance via exfoliation of infected bladder cells, but prolonged TNFɑ signaling exacerbated inflammation, thereby worsening infection. Host genetics and disease history impacts susceptibility by regulating the kinetics of a common TNFɑ pathway.
2019-07-21 | GSE117532 | GEO
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.
2022-05-20 | GSE203195 | GEO
Project description:Viable Candida glabrata cells were co-cultured with pulmonary ILCs. The culture supernatants were collected, cleared of cells and debris, and subsequently precipitated. The precipitated proteins were then analyzed using LC-MS.
2026-02-16 | PXD061271 | Pride
Project description:Uropathogenic Escherichia coli (UPEC) are the most common cause of urinary tract infection (UTI). UPEC normally reside in the intestine, and during establishment of UTI, it undergoes metabolic adaptations, first to urine and then upon tissue invasion to the bladder cell interior. In order to understand these adaptations, we used quantitative proteomic profiling to characterize protein expression of UPEC strain UTI89 growing in human urine and when inside J82 bladder cells. In order to facilitate detection of UPEC proteins over the excess amount of eukaryotic proteins in bladder cells, we developed a method where proteins from UTI89 grown in MOPS and urine was spiked-in to enhance detection of bacterial proteins. More than 2000 E. coli proteins were detected. During growth in urine, proteins associated with iron acquisition and several amino acid uptake and biosynthesis systems, in particular arginine metabolism, were significantly upregulated. During growth in J82 cells, proteins related to iron uptake and arginine metabolisms were upregulated together with proteins involved in sulphur compound turnover. Results suggested that UPEC experience a richer environment in bladder cells compared to urine. There was no direct correlation between upregulated proteins and proteins reported to be essential for infections, showing that upregulation during growth does not signify that the proteins are essential for growth under a condition.
2022-06-09 | PXD032049 | Pride
Project description:Single cell RNAseq of human ILCs to investigate potential heterogeneity within ILC subsets
2019-07-01 | GSE114396 | GEO
Project description:To explore the classification and functional roles of bladder immune cells during urinary tract infection (UTI), we performed scRNA-seq analysis of immune cells extracted from mouse bladders.
2024-10-20 | GSE260501 | GEO
Project description:Obesity is a significant public health concern associated with increased infection risk, but the mechanisms remain unclear. Using a diet induced obesity mouse model, we investigate how obesity impacts urinary tract infection (UTI) susceptibility and bladder urothelial defenses. High fat diet-fed female and male C57BL/6 mice exhibit increased susceptibility to uropathogenic E. coli (UPEC) following experimental UTI. Transcriptomic analysis of bladder urothelial cells reveals sex-specific gene expression changes, but both sexes share activation of focal adhesion and extracellular matrix signaling. Western blot and immunostaining confirm activation of focal adhesion kinase (FAK), a central component of the focal adhesion pathway, in the bladders of obese female and male mice. Mechanistically, primary human urothelial cells overexpressing FAK exhibit increased UPEC invasion. These findings demonstrate that obesity enhances UTI susceptibility and identify FAK as a conserved pathway disrupted by obesity, contributing to increased UPEC vulnerability.
2025-09-19 | GSE294660 | GEO