Ontology highlight
ABSTRACT:
PROVIDER: PRJNA603836 | ENA |
REPOSITORIES: ENA
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Project description:Characterization of violacein-producing bacteria and related species.
| PRJNA738958 | ENA
Project description:Violacein, an indole-derived purple-colored natural pigment isolated from Chromobacterium violaceum has shown multiple biological activities. In this study, we report that violacein activates murine macrophages through the up-regulation of TNF-α expression at non-cytotoxic concentrations (2 µmol/L). This was evaluated by measurement of TNF-α expression using real-time qRT-PCR. In addition, we obtained evidence of the molecular mechanism of activation by determining the mRNA expression pattern upon treatment with violacein. Interestingly, the mRNA expression pattern also allowed us to observe that incubation with violacein caused activation of pathways related with an immune and inflammatory response. Together, our data indicate that violacein activates the TLR8 receptor signaling pathway, and in consequence induces production of inflammatory cytokines such as TNF-α, CCL3 and CCL4 and of negative regulators of TLR signaling such as AP20, IRG1, IκBα and IκBε. Finally, we studied the interaction of TLR8 with violacein in silico, and obtained evidence that violacein could bind to TLR8 in a similar fashion to imidazoquinoline compounds. Therefore, our results indicate that violacein could be a candidate to be applied in immune therapy.
2019-09-25 | GSE82136 | GEO
Project description:Unknown- violacein producing organism genome sequencing
| PRJNA263294 | ENA
Project description:Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf, and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.
2022-09-27 | GSE205142 | GEO
Project description:Two microbial organisms, one violacein producing strains (mixed) Genome sequencing
| PRJNA327982 | ENA
Project description:CurrentNeonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels was observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf, and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathological of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.
2022-09-27 | GSE205143 | GEO
Project description:Some soil bacteria promote plant growth, including Pseudomonas species. With this approach we detected significant changes in Arabidopsis genes related to primary metabolism that were induced by the bacteria.
2010-10-07 | GSE24552 | GEO
Project description:Genome sequencing of BoNT-producing Clostridia and closely related bacteria
| PRJNA391949 | ENA
Project description:Choline is a water-soluble nutrient essential for human life. Gut microbial metabolism of choline results in the production of trimethylamine (TMA), which upon absorption by the host is converted in the liver to trimethylamine N-oxide (TMAO). Recent studies revealed that TMAO exacerbates atherosclerosis in mice, and positively correlates with the severity of this disease in human. However, which microbes contribute to TMA production in the human gut; the extent to which host factors, e.g., genotype and diet, affect TMA production and colonization of these microbes; as well as the effects TMA-producing microbes have on bioavailability of dietary choline remain largely unknown. We screened a collection of 78 sequenced human intestinal isolates encompassing the major phyla found in the human gut and identified eight strains capable of producing TMA from choline in vitro. Gnotobiotic mouse studies showed that TMAO accumulates in the serum of animals colonized with TMA-producing species, but not in the serum of animals colonized with intestinal isolates that do not generate TMA from choline in vitro. Remarkably, low levels of colonization of TMA-producing bacteria significantly reduced choline levels available to the host. This effect was more pronounced as the abundance of TMA-producing bacteria increased. Our findings provide a framework for designing strategies aimed at changing the representation or activity of TMA-producing bacteria in the human gut and suggest the TMA producing status of the gut microbiota should be considered when making recommendations about choline intake requirements for humans.
2015-04-02 | GSE63461 | GEO