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Differential tissue-specific damage caused by bacterial epididymo-orchitis in the mouse.

ABSTRACT: Differential tissue-specific damage caused by bacterial epididymo-orchitis in the mouse.

PROVIDER: PRJNA591923 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10539857.fastq.gz	Fastqsanger.gz
	SRR10539858.fastq.gz	Fastqsanger.gz
	SRR10539859.fastq.gz	Fastqsanger.gz
	SRR10539860.fastq.gz	Fastqsanger.gz
	SRR10539861.fastq.gz	Fastqsanger.gz

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Differential tissue-specific damage caused by bacterial epididymo-orchitis in the mouse.

Project description:This study investigated the differential responses of the epididymis and testis to infection with uropathogenic Escherichia coli (UPEC) in adult mice. In contrast to the cauda epididymidis, which exhibited ongoing damage following UPEC-infection, spermatogenic disruption was reversible and the caput epididymidis was largely unaffected. The caput epididymidis is structurally and functionally very different from the cauda, whereas beta-defensins as important epididymal antimicrobial factors are highly expressed in both tissues. The transcriptome of the testis, caput, corpus and cauda epididymidis were analysed in normal, wildtype C57BL/6J mice. Distinct differences in gene signatures were observed between caput and cauda epididymidis, particularly among immune-related genes, whereas corpus and cauda were much more alike. Beta-defensins were found at high levels in both caput and cauda epididymidis, whereas other antimicrobial factors, such as Lipocalin 2 and Lypd8 were found expressed selectively high in the caput epididymidis and hence may play an important role in local protection from bacterial pathogens, including UPEC.

2020-05-06 | GSE141071 | GEO

Differential tissue-specific damage caused by bacterial epididymo-orchitis in the mouse.

Project description:Ascending bacterial urinary tract infections can cause epididymo-orchitis. In the cauda epididymidis, this frequently leads to persistent tissue damage. Less coherent data is available concerning the functional consequences of epididymo-orchitis on testis and caput epididymidis. This in vivo study addresses the functional and spatial differences in responsiveness of murine epididymis and testis to infection with uropathogenic Escherichia coli (UPEC). Whole transcriptome analysis (WTA) was performed on testis, caput, corpus and cauda epididymidis of adult C57BL/6 J wildtype mice. Following UPEC-induced epididymo-orchitis in these mice, epididymal and testicular tissue damage was evaluated histologically and semi-quantitatively at 10 days and 31 days post-inoculation. Expression of inflammatory markers and candidate antimicrobial genes were analysed by RT-qPCR. WTA revealed distinct differences in gene signatures between caput and cauda epididymidis, particularly amonst immunity-related genes. Cellular and molecular signs of testicular inflammation and disruption of spermatogenesis were noticed at day 10, but recovery was observed by day 31. In contrast to the cauda, the caput epididymidis did not reveal any signs of gross morphological damage or presence of pro-inflammatory processes despite confirmed infection. In contrast to beta-defensins, known UPEC-associated antimicrobial peptides (AMP), like Lcn2, Camp and Lypd8, were inherently highly expressed or upregulated in the caput following infection, potentially allowing an early luminal protection from UPEC. At the time points investigated, the caput epididymidis was protected from any obvious infection/inflammation-derived tissue damage. Studies addressing earlier time-points will conclude whether in the caput epididymidis a pro-inflammatory response is indeed not essential for effective protection from UPEC.

| S-EPMC7187874 | biostudies-literature

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

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

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

| PRJNA863301 | ENA

Differential expression caused by Dicer knockout in small intestine

Project description:This SuperSeries is composed of the following subset Series: GSE34905: Differential gene expression caused by Dicer knockout in small intestine GSE34909: Differential miRNA expression caused by Dicer knockout in small intestine Refer to individual Series

2012-01-07 | E-GEOD-34910 | biostudies-arrayexpress

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

miRNA profile of duck duodenum mucosa damage caused by oxidative stress

Project description:miRNA profile of duck duodenum mucosa damage caused by oxidative stress

| PRJNA996064 | ENA

miRNA profile of duck duodenum mucosa damage caused by transportation stress

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Gut epithelial barrier damage caused by dishwasher detergents and rinse aids

Project description:Gut epithelial barrier damage caused by dishwasher detergents and rinse aids

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Inhibition of IL-6 signaling attenuates vascular damage caused by HIF1α activation

Project description:Inhibition of IL-6 signaling attenuates vascular damage caused by HIF1α activation