Microbiota-derived acetate protects against UPEC-epididymo-orchitis by improving the phagocytosis of testicular macrophages.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1184345 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31302976_1.fastq.gz | Fastqsanger.gz | |||
| SRR31302976_2.fastq.gz | Fastqsanger.gz | |||
| SRR31302977_1.fastq.gz | Fastqsanger.gz | |||
| SRR31302977_2.fastq.gz | Fastqsanger.gz | |||
| SRR31302978_1.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Ascending bacterial infections of the male genitourinary tract by Escherichia coli are an important cause of male infertility. Thus understanding mechanisms by which immunocompetent cells such as testicular macrophages (TM) respond to infection and how bacterial pathogens manipulate defense pathways is of great relevance. Following infection with uropathogenic E. coli (UPEC) whole genome expression profiling revealed induction of the calcium-dependent nuclear factor of activated T cells (NFAT) signaling pathway in TM as well as in peritoneal macrophages (PM) that were used in comparison. UPEC-dependent NFAT activation was confirmed in cultured TM and in TM using an in vivo infection model. Elevated expression of NFATC2-regulated anti-inflammatory cytokines was found in TM (IL-4, IL-13) and PM (IL-3, IL-4, IL-13). NFATC2 is activated by a rapid influx of calcium caused by the UPEC pore forming toxin alpha-hemolysin. Mutant analysis identified alpha-hemolysin as the main virulent factor responsible for UPEC-dependant suppression of IL-6 and TNF-a cytokine release from PM. Alpha-hemolysin caused differential activation of MAP kinase and AP-1 signaling pathways in TM and PM leading to differential expression profiles of key pro-inflammatory cytokines in PM (IL-1a, IL-1b and IL-6 downregulated) and TM (IL-1b and IL-6 upregulated). In contrast to PM, treatment with lipopolysaccharide did not result in activation of the NFkB pathway in TM as shown by lack of degradation of IkBa and lack of pro-inflammatory cytokine secretion (IL-6, TNF-a). In conclusion, these results propose a mechanism how TM can defend against microbes, while at the same time they are able to maintain the immune privileged status of the testis. 2 Macrophage populations ( peritoneal, testicular) infected with UPEC CFT073; timepoints of mrna harvest at 0 min (control), 30 min and 60 min; of each point 2 biological replicates; of each repliccate 2 technical replicates: summa summarum: 2*((1+1+1)*2*2)=24 samples
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Project description:Ascending bacterial infections of the male genitourinary tract by Escherichia coli are an important cause of male infertility. Thus understanding mechanisms by which immunocompetent cells such as testicular macrophages (TM) respond to infection and how bacterial pathogens manipulate defense pathways is of great relevance. Following infection with uropathogenic E. coli (UPEC) whole genome expression profiling revealed induction of the calcium-dependent nuclear factor of activated T cells (NFAT) signaling pathway in TM as well as in peritoneal macrophages (PM) that were used in comparison. UPEC-dependent NFAT activation was confirmed in cultured TM and in TM using an in vivo infection model. Elevated expression of NFATC2-regulated anti-inflammatory cytokines was found in TM (IL-4, IL-13) and PM (IL-3, IL-4, IL-13). NFATC2 is activated by a rapid influx of calcium caused by the UPEC pore forming toxin alpha-hemolysin. Mutant analysis identified alpha-hemolysin as the main virulent factor responsible for UPEC-dependant suppression of IL-6 and TNF-a cytokine release from PM. Alpha-hemolysin caused differential activation of MAP kinase and AP-1 signaling pathways in TM and PM leading to differential expression profiles of key pro-inflammatory cytokines in PM (IL-1a, IL-1b and IL-6 downregulated) and TM (IL-1b and IL-6 upregulated). In contrast to PM, treatment with lipopolysaccharide did not result in activation of the NFkB pathway in TM as shown by lack of degradation of IkBa and lack of pro-inflammatory cytokine secretion (IL-6, TNF-a). In conclusion, these results propose a mechanism how TM can defend against microbes, while at the same time they are able to maintain the immune privileged status of the testis.
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Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female CBA mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice
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Project description:We report the application of H3 Lysine9 acetylation (H3K9ac) immunoprecipitation coupled next generation sequencing (ChIP-seq) in human bladder epithelial cells 5637 following treatment with Urophathogenic Escherichia coli strain 536 (UPEC) or the mutant with deletion of both α-hemolysin (hlyA) genes in the UPEC 536 strain (hlyA double mutant = UPEC 536 HDM) or UPEC supplemented with acetate. We found dramatic depletion of H3K9ac peaks was observed in UPEC infected cells, which was partially rescued by supplementation of acetate. In contrast, H3K9ac peaks of untreated cells are comparable with HDM treated cells. A total 21834 merged peak regions were identified in untreated control, whilst UPEC infection significantly decreased the signal across the merged peak regions, which was rescued partially by adding acetate. Deacetylation and its rescue by addition of acetate were observed in a global manner and affected the vast majority of H3K9ac sites throughout the genome. This observation holds true for different classes of cis-regulatory elements. Analysis of average binding across all human transcriptional start sites analysis further revealed that UPEC treatment also decrease H3K9ac signals at promoter regions, and can be rescue by supplementation of acetate. Moreover H3K9ac signal is also correlated with gene expression pattern. This study established that UPEC infection could epigenetically manipulate the host cell gene expression.
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Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female CBA mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice Whole mouse bladder collected at 2h following transurethral infection for RNA extraction and hybridization on Affymetrix microarrays. Non-pooled samples were used, with one array per mouse to expand power of expression profiles. Control mice received only PBS as a mock infection. Group sizes were five mice per group, and therefore five arrays were used per group.
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Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female C57BL/6 mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice Whole mouse bladder collected at 2h following transurethral infection for RNA extraction and hybridization on Affymetrix microarrays. Non-pooled samples were used, with one array per mouse to expand power of expression profiles. Control mice received only PBS as a mock infection. Group sizes were five mice per group, and therefore five arrays were used per group.
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