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Activin A and CCR2 regulate the function of macrophages in testicular fibrosis caused by experimental autoimmune orchitis

ABSTRACT: Activin A and CCR2 regulate the function of macrophages in testicular fibrosis caused by experimental autoimmune orchitis

PROVIDER: PRJNA863301 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20698368.fastq.gz	Fastqsanger.gz
	SRR20698369.fastq.gz	Fastqsanger.gz
	SRR20698370.fastq.gz	Fastqsanger.gz
	SRR20698371.fastq.gz	Fastqsanger.gz
	SRR20698372.fastq.gz	Fastqsanger.gz

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Similar Datasets

Activin A and CCR2 regulate the function of macrophages in testicular fibrosis caused by experimental autoimmune orchitis

Project description:Treatment of bone marrow-derived macrophages with activin A in vitro increased the expression of Ccr2, Fn1, Cxcr4, and Mmp2 and these effects were abolished by follistatin.

2024-04-19 | GSE210004 | GEO

Activin A and CCR2 regulate macrophage function in testicular fibrosis caused by experimental autoimmune orchitis.

Project description:Experimental autoimmune-orchitis (EAO), a rodent model of chronic testicular inflammation and fibrosis, replicates pathogenic changes seen in some cases of human spermatogenic disturbances. During EAO, increased levels of pro-inflammatory and pro-fibrotic mediators such as TNF, CCL2, and activin A are accompanied by infiltration of leukocytes into the testicular parenchyma. Activin A levels correlate with EAO severity, while elevated CCL2 acting through its receptor CCR2 mediates leukocyte trafficking and recruits macrophages. CCR2 + CXCR4 + macrophages producing extracellular matrix proteins contribute widely to fibrogenesis. Furthermore, testicular macrophages (TMs) play a critical role in organ homeostasis. Therefore, we aimed to investigate the role of the activin A/CCL2-CCR2/macrophage axis in the development of testicular fibrosis. Following EAO induction, we observed lower levels of organ damage, collagen deposition, and leukocyte infiltration (including fibronectin+, collagen I+ and CXCR4+ TMs) in Ccr2-/- mice than in WT mice. Furthermore, levels of Il-10, Ccl2, and the activin A subunit Inhba mRNAs were lower in Ccr2-/- EAO testes. Notably, fibronectin+ TMs were also present in biopsies from patients with impaired spermatogenesis and fibrotic alterations. Overexpression of the activin A antagonist follistatin reduced tissue damage and collagen I+ TM accumulation in WT EAO testes, while treating macrophages with activin A in vitro increased the expression of Ccr2, Fn1, Cxcr4, and Mmp2 and enhanced migration along a CCL2 gradient; these effects were abolished by follistatin. Taken together, our data indicate that CCR2 and activin A promote fibrosis during testicular inflammation by regulating macrophage function. Inhibition of CCR2 or activin A protects against damage progression, offering a promising avenue for therapeutic intervention.

| S-EPMC9700630 | biostudies-literature

Microbiota-derived acetate protects against UPEC-epididymo-orchitis by improving the phagocytosis of testicular macrophages.

Project description:The gut microbiota is intimately associated with maintaining a stable intestinal immune balance. However, it remains unclear whether gut dysbiosis affects the homeostasis within the testes. In our DSS-induced colitis mouse model, we observed increased inflammatory cell infiltration within the mouse testes. Analysis of the gut microbiota in the feces of DSS colitis mice and mice treated with antibiotics revealed a significant decrease in the number of bacteria related to cellulose decomposition in the gut, as well as a decrease in the content of short-chain fatty acid salts in the peripheral blood of mice. In vitro experiments found that acetate can significantly improve the outcome of UPEC-induced bacterial epididymo-orchitis. Further in vitro experiments demonstrated that acetate can enhance the bacterial phagocytic ability of testicular macrophages (TM), accelerate the early clearance of bacteria within the testes, and thus reduce the degree of testicular inflammation. This study provides a link to explain the progression of bacterial epididymo-orchitis in relation to gut microbiota dysbiosis and offers new insights for the treatment of bacterial epididymo-orchitis.

2025-05-01 | GSE281537 | GEO

Fluvastatin protects Leydig cells in orchitis through direct activation of Peroxiredoxin 1

Project description:Orchitis caused by infection is one of the most important causes of male infertility, which can cause an imbalance of the oxidation/antioxidation system. Appropriate antioxidant therapy may be effective in alleviating testicular damage. Previous studies found that peroxiredoxin 1 (PRDX1) is involved in the regulation of oxidative stress and inflammation, and is highly expressed in testis. Therefore, selecting an effective PRDX1 agonist might become an attractive strategy in the treatment of orchitis related to oxidative stress. In the current study, we identified the effective agonist of PRDX1. Leydig cells were used to find the antioxidant role and mechanisms of the agonist in vitro. Models of orchitis in wild-type and Prdx1-/- mice were employed to confirm the anti-orchitis effect of the agonist. We found that fluvastatin (FV), a classical cholesterol-lowering drug, could directly bind PRDX1 to activate its enzyme activity. FV played a protective and antioxidant role on H2O2-treated Leydig cells by improving cell viability and testosterone level, inhibiting apoptosis, and reducing reactive oxygen species level and inflammatory factors in a PRDX1-dependent manner. FV could also decrease oxidative stress and inflammation levels of testes in mice models, thereby reducing the damage on testicular steroidogenesis and spermatogenesis caused by orchitis. FV was an effective agonist of PRDX1, which showed antioxidant and anti-inflammatory impact in orchitis. Our results may shed light on the antioxidant treatment of orchitis and male infertility.

2025-12-03 | GSE298181 | GEO

Testicular activin and follistatin levels are elevated during the course of experimental autoimmune epididymo-orchitis in mice.

Project description:Experimental autoimmune epididymo-orchitis (EAEO) is a model of chronic inflammation, induced by immunisation with testicular antigens, which reproduces the pathology of some types of human infertility. Activins A and B regulate spermatogenesis and steroidogenesis, but are also pro-inflammatory, pro-fibrotic cytokines. Expression of the activins and their endogenous antagonists, inhibin and follistatin, was examined in murine EAEO. Adult untreated and adjuvant-treated control mice showed no pathology. All mice immunised with testis antigens developed EAEO by 50 days, characterised by loss of germ cells, immune cell infiltration and fibrosis in the testis, similar to biopsies from human inflamed testis. An increase of total CD45+ leukocytes, comprising CD3+ T cells, CD4 + CD8- and CD4 + CD25+ T cells, and a novel population of CD4 + CD8+ double positive T cells was also detected in EAEO testes. This was accompanied by increased expression of TNF, MCP-1 and IL-10. Activin A and B and follistatin protein levels were elevated in EAEO testes, with peak activin expression during the active phase of the disease, whereas mRNA expression of the inhibin B subunits (Inha and Inhbb) and activin receptor subunits (Acvr1b and Acvr2b) were downregulated. These data suggest that activin-follistatin regulation may play a role during the development of EAEO.

| S-EPMC5304336 | biostudies-literature

CCR2+ vs. CCR2- murine hematopoietic stem cells

Project description:Comparative analysis of FACS-sorted CCR2- and CCR2+ HSC in the steady state. CCR2+ HSC have fourfold higher proliferative rates than CCR2- HSC, are are biased towards the myeloid lineage and dominate the migratory HSC population. Comparison of pooled CCR2- and CCR2+ HSC (bone marrow from 20 mice pooled for each sample), three biological replicates each.

2015-05-01 | E-GEOD-53827 | biostudies-arrayexpress

Microbiota-derived acetate protects against UPEC-epididymo-orchitis by improving the phagocytosis of testicular macrophages.

Project description:Microbiota-derived acetate protects against UPEC-epididymo-orchitis by improving the phagocytosis of testicular macrophages.

| PRJNA1184345 | ENA

CCR2+ vs. CCR2- murine hematopoietic stem cells

2015-05-01 | GSE53827 | GEO

single-cell analysis of experimental autoimmune orchitis (EAO) in mice

Project description:single-cell analysis of experimental autoimmune orchitis (EAO) in mice

| PRJNA761421 | ENA

Transcriptome comparison between CCR2+ and CCR2- classical monocytes in SIV-infected Macaca nemestrina

Project description:Monocytes have been categorized in three main subpopulations based on CD14 and CD16 surface expression. Classical monocytes are the most abundant subset in the blood. They express a CD14+CD16-CCR2+ phenotype, which confers on them the ability to migrate to inflammatory sites by quickly responding to CCL2 signaling. Here we identified and characterized the surge and expansion of a novel monocyte subset during SIV and HIV infection. They were undistinguishable from classical monocytes regarding CD14 and CD16 expression, but did not express surface CCR2. Transcriptome analysis of sorted cells confirmed that they represent a distinct subpopulation that expresses lower levels of inflammatory cytokines and activation markers than their CCR2+ counterparts. They exhibited impaired phagocytosis and deficient chemotaxis in response to CCL2 and CCL7, besides being refractory to SIV infection. We named these cells atypical CCR2- classical (ACC) monocytes, and believe they play an important role in AIDS pathogenesis, possibly reflecting an anti-inflammatory response against the extreme immune activation observed during SIV and HIV infection. Antiretroviral therapy caused this population to decline in both macaque and human subjects, suggesting that this atypical phenotype may be induced by viral replication. Expression profiling by NanoString nCounter gene expression system. Classical monocytes (CD14++CD16-) from six SIV-infected macaques (day 14 post inoculation) were sorted in two groups according to CCR2 expression.

2012-03-01 | E-GEOD-27559 | biostudies-arrayexpress

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