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Single-Cell RNA sequencing reveals the immune microenvironment and signaling networks in cystitis glandularis

ABSTRACT: Single-Cell RNA sequencing reveals the immune microenvironment and signaling networks in cystitis glandularis

PROVIDER: PRJNA934318 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23444900_1.fastq.gz	Fastqsanger.gz
	SRR23444900_2.fastq.gz	Fastqsanger.gz
	SRR23444901_1.fastq.gz	Fastqsanger.gz
	SRR23444901_2.fastq.gz	Fastqsanger.gz
	SRR23444902_1.fastq.gz	Fastqsanger.gz

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Single-Cell RNA sequencing reveals the immune microenvironment and signaling networks in cystitis glandularis

Project description:Cystitis glandularis (CG) is a common chronic bladder hyperplastic disease. The current lack of unified diagnosis and treatment criteria makes it essential to comprehensively describe the inflammatory immune environment in CG research. Here, we performed scRNA-sequencing in CG patients for the first time, in which four inflamed tissues as well as three surrounding normal bladder mucosa tissues were included. Specifically, we isolated 18,869 cells to conduct bioinformatic analysis and performed immunofluorescence experiments. Our genetic results demonstrate that CG does not have the classic chromosomal variation observed in bladder tumors, reveal the specific effects of TNF in KRT15 epithelial cells, and identify a new population of PIGR epithelial cells with high immunogenicity. In addition, we confirmed the activation difference of various kinds of T cells during chronic bladder inflammation and discovered a new group of CD27-Switch memory B cells expressing a variety of immunoglobulins. Our study reveals, for the first time, the different kinds of cell subgroups in CG and provides the necessary basis for the clinical treatment of cystitis glandularis.

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Project description:Cystitis is a bacterial infection of the bladder that occurs in about half of women at least once in their lifetime. Antibiotics such as nitrofurantoin are used to treat cystitis but antibiotic resistance is a concern, especially for recurrent infections. Here we report an open label, randomized, single-center, phase 2 study to analyze the acute and long-term safety and efficacy of the IL-1 receptor antagonist anakinra, compared to nitrofurantoin, in recurrent cystitis. Thirty adult female patients with a documented history of recurrent cystitis and a current acute cystitis episode were randomized in a 2:1 ratio to treatment with anakinra (n=20) or nitrofurantoin (n=10) for five days. Primary and secondary efficacy end points were reached, defined as the reduction in typical symptoms, measured by the acute cystitis symptom score (ACSS, day 5), longitudinal symptom scores, recurrence rates, quality of life gene, expression analysis and microbiology at follow-up on days 15, 30 and at six months. Symptom scores were decreased in the anakinra (P<0.001), and nitrofurantoin (P<0.001) arms after five days and remained low after 15, 30 days and 6 months. Recurrences were less frequent after 6 months in both treatment groups compared to the 6-month pre-enrolment history (P<0.001 for anakinra and P=0.004 for nitrofurantoin) and the quality of life was increased, without adverse effects. Immune gene expression was rapidly inhibited in the anakinra treated patients but not in the nitrofurantoin group. Targeted innate immune inhibition therapy shows non-inferiority to nitrofurantoin in patients with recurrent acute cystitis (German Clinical Trials Register, DRKS00025964; EudraCT, 2019-004209-28).

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Single-cell RNA sequencing reveals the immune microenvironment and signaling networks in cystitis glandularis.

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Dysregulated miRNAs modulate tumor microenvironment associated signaling networks in pancreatic ductal adenocarcinoma

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Project description:Hormone receptor–positive (HR⁺) breast cancers comprise ~80% of breast cancer cases, yet endocrine resistance remains a clinical barrier. While estrogen receptor alpha (ER) biology is well characterized, the role of progesterone receptor (PR) signaling in tumor progression and immune evasion is less defined. Using the ER⁺/PR⁺ SSM2 murine mammary tumor model, we investigated progesterone’s influence on tumor growth and the immune microenvironment. Progesterone significantly accelerated tumor growth in vivo and enhanced proliferation in vitro. Single-cell RNA sequencing (scRNA-seq) revealed that progesterone treatment reshaped the tumor microenvironment, expanding the tumor cell compartment while markedly reducing immune populations. Tumor-intrinsic analyses showed downregulation of interferon and antigen presentation pathways, alongside upregulation of cell cycle and proliferation signaling. Within the immune compartment, progesterone reduced overall T cell infiltration, shifted CD4⁺ T cells toward a regulatory phenotype, and increased macrophages. Notably, lipid-associated macrophages (LAMs) with a high Apoe/Trem2 signature were markedly expanded and engaged in immunosuppressive Spp1–CD44 signaling with immune cells. CellChat analysis of inferred ligand–receptor interactions revealed LAM-driven communication networks that may impair the anti-tumor immune response. Analysis of human breast cancer scRNA-seq datasets confirmed that PRhi tumors harbored more LAMs than PRlo tumors, supporting the translational relevance of our findings. Collectively, these data establish progesterone signaling as a driver of immune suppression in HR⁺ breast cancer through coordinated effects on tumor cells, T cells, and macrophages. Targeting PR signaling or LAM subsets may represent novel therapeutic strategies to overcome immune evasion and sensitize HR⁺ tumors to immunotherapy.

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