The role of queuine as a nutritional regulator of the response of Entamoeba histolyticato oxidative stress
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA596228 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Amebiasis is an intestinal disease transmitted by the protist parasite, Entamoeba histolytica, following the ingestion of contaminated food and water. Many infected patients (90%) are asymptomatic but for unknown reasons, these trophozoites can become virulent and invasive, cause amebic dysentery, and migrate to the liver, via the portal veins, where they cause hepatocellular damage. We have recently reported that Escherichia coli can modulate E.histolytica 's virulence and resistance to oxidative stress (OS) via the production of oxaloacetate. Queuosine is a naturally occurring modified nucleoside and is found in the first position of the anticodon of the transfer RNAs for Asp, Asn, His and Tyr. Lower and higher eukaryotes are supplied with queuine (the base of queuosine) in the diet or by the intestinal flora. Here, we have tested the hypothesis that queuine being a micronutrient offers an advantage to E.histolytica during OS. Queuine which is efficiently incorporated in E.histolytica’s tRNAs leads to significant modifications of the parasite’s transcriptome, to hypermethylation of C38 in tRNAAspGTC and consequently to OS resistance. While queuine leads to the translation of proteins during OS, we found that that it inhibits protein synthesis otherwise. Localization studies with an antibody against EhTGT in queuine-treated trophozoites revealed the presence of small granular structures. We have biochemically characterized the parasite’s tRNA-guanine transglycosylase (TGT), the enzyme that catalyzes the modification of Q-tRNAs. Trophozoites silenced for TGT expression have a growth defect and they are less resistant to OS compared to control trophozoites.
2021-02-18 | GSE142211 | GEO
Project description:Enteric bacteria increase the defenses against oxidative stress in Entamoeba histolytica
| PRJNA412624 | ENA
Project description: Not available
| S-EPMC8092309 | biostudies-literature
Project description:Characterization of the human microbiota is providing new insightsinto the complexity of host–parasite–bacterium relationships. Amoebiasis (an intestinal infection affecting a large proportion of the population in many countries worldwide) is caused by the amoebic parasite Entamoeba histolytica. During amoebiasis, the parasite encounters several types of stress as a result of the host’s response to infection. Given that E. histolytica phagocytises bacteria in the intestinal lumen, we hypothesized that enteric bacteria can influence the course of an amoebic infection. Hence, we used live Escherichia coli O55 as a pertinent model of the bacterial community’s contribution to amoebic responses during host- induced stress. By measuring amoebic survival, we found that live E. coli protected E. histolytica against oxidative stress (OS) but not against nitrosative stress. E. coli– associated protection is correlated with massive transcriptionalchanges in amoebic genes acquired through lateral transfer from the bacterial kingdom, including genes coding for proteinscontaining leucine-rich repeat (LRR) motifs. The transcriptome profile triggered by OS and E. coli was also observed with other enteric bacteria, including pathogens and non-pathogens. In contrast, exposure to a probiotic resulted in a different transcriptome profile. The present study shows that OS and live bacteria together modulate 84 of E. histolytica’s 137 LRR protein genes. The LRR proteins are involvedin protein-ligand and protein-protein interactions – especially in proteins that interact with bacteria as part of the innate immune response in mammals and plants, such as Toll-like receptors. The structural and functional homology of LRRs and TLRs identified here suggest that despite its old age in evolutionary terms, the protozoan E. histolytica displays key characteristics of higher eukaryotes’ innate immune systems. We conclude that components of innate immunity existed in the common ancestor of plants and animals
2018-06-08 | GSE104434 | GEO
Project description:Campylobacter jejuni is the leading bacterial cause of human gastroenteritis worldwide. Despite stringent microaerobic growth requirements, C. jejuni is ubiquitous in the aerobic environment. C. jejuni must possess finely tuned regulatory systems to sense and adapt to external stimuli such as oxidative and aerobic (O2) stress. Re-annotation of the C. jejuni NCTC11168 genome sequence identified Cj1556 (originally annotated as a hypothetical protein) as a MarR family transcriptional regulator and further bioinformatic analysis indicated a role in regulating the oxidative stress response. A C. jejuni 11168H Cj1556 mutant exhibited increased sensitivity to oxidative and aerobic stress, decreased ability for intracellular survival in both Caco-2 human intestinal epithelial cells and J774A.1 mouse macrophages and a reduction in virulence in the Galleria mellonella infection model. Microarray analysis of gene expression changes in the Cj1556 mutant compared to the wild-type strain indicated negative autoregulation of Cj1556 expression and down-regulation of genes associated with oxidative and aerobic stress responses, such as katA, perR and hspR. cprS, which encodes a sensor kinase involved in the regulation of biofilm formation, was also up-regulated in the Cj1556 mutant and subsequent studies showed that the Cj1556 mutant had a reduced ability to form biofilms. Protein interaction studies confirmed the binding of recombinant Cj1556 to a region upstream of Cj1556. This study has identified a novel C. jejuni transcriptional regulator Cj1556 that is involved in oxidative and aerobic stress responses and is important for the survival of C. jejuni in the natural environment and in vivo. This newly identified regulator was designated CosR (Campylobacter oxidative stress Regulator). Data is also available from <ahref=""http://bugs.sgul.ac.uk/E-BUGS-119"" target=""_blank"">BuG@Sbase</a>
2012-01-23 | E-BUGS-119 | biostudies-arrayexpress
Project description:BACH1, the master regulator of oxidative stress, modulates CFTR gene expression
| PRJNA695525 | ENA
Project description:Differential expression was used to access gene differences after Entamoeba histolytica infection. Entamoeba histolytica is an important diarrheal pathogen worldwide, and induces apoptosis of the intestinal epithelium as part of its disease process. Regenerating (REG) 1 protein is anti-apoptotic. We investigated the involvement of REG 1 in E. histolytica colitis. Colonic biopsy samples were obtained from 8 subjects with acute E. histolytica colitis, and again 60 day later during convalescence. Gene expression in the human colon during acute and convalescent E. histolytica disease was evaluated using microarray and confirmed by polymerase chain reaction (PCR). REG 1 protein expression was evaluated with immunohistochemistry. The mechanism of REG 1 involvement in E. histolytica disease was subsequently investigated with a mouse model. REG 1A and REG 1B were the most upregulated genes in the human intestine in acute versus convalescent E. histolytica disease (p=0.003 and p=0.006 respectively). PCR confirmed the microarray results (p=<0.001 and p=0.001 respectively). Increased REG 1A and REG 1B protein expression was similarly observed by immunohistochemistry. REG 1 -/-mice were found to be significantly more susceptible to E. histolytica infection than wild type mice.
2011-05-24 | GSE23750 | GEO
Project description:Entamoeba histolytica is a protozoan parasite which causes colitis and liver abscesses. Using a genomic DNA microarray consisting of 1.6 - 2.0 kb genomic inserts we have generated a transcriptional profile of 1,971 unique parasite transcripts. The arrays in this experiment set were used to (1) estimate relative transcript abundance for Entamoeba histolytica (HM-1:IMSS) trophozoites in mid-logarithmic growth and (2) to examine changes in the transcriptional profile of Entamoeba histolytica when the parasite interacts with colonic epithelial cells (Caco-2). A time course was used such that RNA was isolated from ameba alone and ameba + Caco-2 cells at 3hrs, 6hrs and 9hrs corresponding to 10%, 50% and 90% cell monolayer destruction. At least two biological experiments and three replicates were used for each time point. Groups of assays that are related as part of a time series. Keywords: time_series_design
2005-07-22 | GSE2979 | GEO
Project description:The transcriptional regulator CCCTC-binding factor limits oxidative stress in endothelial cells
| PRJNA431261 | ENA
Project description:Francisella tularensis is a Gram-negative bacterium that causes a fatal human disease known as tularemia. The Centers for Disease Control have classified F. tularensis as Category A Tier-1 Select Agent. The virulence mechanisms of Francisella are not entirely understood. Francisella possesses very few transcription regulators, and most of these regulate the expression of genes involved in intracellular survival and virulence. The F. tularensis genome sequence analysis reveals an AraC (FTL_0689) transcriptional regulator homologous to the AraC/XylS family of transcriptional regulators. In Gram-negative bacteria, AraC activates genes required for L-arabinose utilization and catabolism. The role of the FTL_0689 regulator in F. tularensis is not known. In this study, we characterized the role of FTL_0689 in gene regulation of F. tularensis and investigated its contribution to intracellular survival and virulence. The results demonstrate that FTL_0689 in Francisella is not required for L-arabinose utilization. Instead, FTL_0689 specifically regulates the expression of the oxidative and global stress response, virulence, metabolism, and other key pathways genes required by Francisella when exposed to oxidative stress. The FTL_0689 mutant is attenuated for intramacrophage growth, and mice infected with the FTL_0689 mutant survive better than wild-type F. tularensis LVS infected mice. Based on the deletion mutant phenotype, FTL_0689 was termed osrR (oxidative stress response regulator). Altogether, this study elucidates the role of the osrR transcriptional regulator in tularemia pathogenesis.
2021-10-13 | GSE183001 | GEO