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ABSTRACT: Urinary microbiome of pelvis urine from CaOx stone patients

PROVIDER: PRJNA970228 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24524245.fastq.gz	Fastqsanger.gz
	SRR24524246.fastq.gz	Fastqsanger.gz
	SRR24524247.fastq.gz	Fastqsanger.gz
	SRR24524248.fastq.gz	Fastqsanger.gz
	SRR24524249.fastq.gz	Fastqsanger.gz

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Project description:Urinary tract-associated lymphoid structures (UTLASs), tertiary lymphoid tissues, are formed in renal pelvis (RP) of humans and mice with chronic kidney disease. We found that UTALS development was accelerated by urine leakage from RP lumen to the parenchyma following dysfunction of transitional epithelium covering UTLASs. Thus, UTALS-forming cells were stimulated by urine including urinary bio active substances.

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Project description:Kidney stone disease causes significant morbidity and increases health care utilization. In this dataset, we applied a single-nucleus assay to renal papila samples in order to charachterize the cellular and molecular niches in patients with calcium oxalate (CaOx) stone disease and healthy subjects. In addition to identifying cell types important in papillary physiology, we characterize collecting duct cell subtypes and an undifferentiated epithelial cell type that was more prevalent in stone patients. Despite the focal nature of mineral deposition in nephrolithiasis, we uncover a global injury signature characterized by immune activation, oxidative stress and extracellular matrix remodeling. We also identify the association of MMP7 and MMP9 expression with stone disease and mineral deposition, respectively. MMP7 and MMP9 are significantly increased in the urine of patients with CaOx stone disease, and their levels correlate with disease activity. Our results define the spatial molecular landscape and specific pathways contributing to stone-mediated injury in the human papilla and identify associated urinary biomarkers.

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Project description:Tertiary lymphoid tissues (TLTs) are formed in systemic organs manifesting chronic inflammation. Herein, we found that the renal pelvis (RP) could form urinary tract-associated lymphoid tissues (UTALTs) in a TLT-formation manner in humans and mice with chronic kidney disease (CKD), regardless of infectious pyelonephritis. Our results demonstrated that urine is crucial for UTALT development. Urine leak from the lumen into the parenchyma of the RP through an altered transitional epithelium (TE) barrier, stimulated RP stromal cells immunologically and attracted immune cells via cytokine and chemokine production. Pathophysiological crosstalk was observed between UTALT development and tubulointerstitial lesions and TLT formation in the kidney.

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