Ramlibacter tataouinensis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA35861 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A cyst-producing bacteria from a subsurface desert soil in Tunisia
| PRJNA16294 | ENA
Project description:Indole is an intercellular and interkingdom signaling molecule, which is widespread in diverse ecological niches. Caenorhabditis elegans is a bacterivorous nematode living in soil and compost environments and a useful model host for the study of host-microbe interactions. While various bacteria and some plants produce a large quantity of extracellular indole, little is known about the effects of indole, its derivatives, and indole-producing bacteria on behaviors in C. elegans and animals. Here, we show that C. elegans senses and moves toward indole and indole-producing bacteria, such as Escherichia coli, Shigella boydii, Providencia stuartii, and Klebsiella oxytoca, while avoids non-indole producing pathogenic bacteria. It was also found that indole-producing bacteria and non-indole-producing bacteria exert divergent effects on egg-laying behavior of C. elegans via indole. In addition, various indole derivatives also modulate chemotaxis, egg-laying behavior, and survival of C. elegans. In contrast, indole at a high concentration to kill C. elegans that has the ability to detoxify indole via oxidation and glucosylation, indicating predator-prey interactions via a double-edged molecule indole. Transcriptional analysis showed that indole markedly up-regulated gene expression of cytochrome P450 family, UDP-glucuronosyltransferase, glutathione S-transferase, which explained well the modification of indole in C. elegans, while down-regulated expression of collagen genes and F-box genes. Our findings suggest that indole and its derivatives are important interkingdom signaling molecules in bacteria-nematode interactions.
2019-08-31 | GSE86312 | GEO
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: Not available
| S-EPMC6848086 | biostudies-literature
Project description:Interventions: Colibactin positive patients are given biolactis (3 g/day) for 3 months.
Primary outcome(s): Detection of colibactin-producing bacteria 90 days after the start of the intervention.
Study Design: single arm study, open(masking not used), no treatment control/standard of care control, single assignment, basic science
| 2615357 | ecrin-mdr-crc
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