Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1054188 | ENA |
REPOSITORIES: ENA
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Project description:Biocides are chemical compounds widely used in hospital settings for a variety of purposes, but mainly for disinfection. The chemical properties of a biocide, as well as the biocide concentration, influence which cellular targets are affected. Exposure of bacteria to residual concentrations of biocides could lead to development of increased resistance towards the biocide in use, as well as cross-resistance towards other antimicrobials, including antibiotics. The aim of this study was to examine whether biocides could induce any potentially relevant genes that could affect pathogen's drug resistance or fitness. By examining global gene expression of the uropathogenic Escherichia coli CFT073 after exposure to subinhibitory concentrations of four biocides (benzalkonium chloride - BAC, chlorhexidine - CHX, hydrogen peroxide - H2O2, triclosan - TSN), we found that each biocide changed expression of different groups of genes and that exposure to benzalkonum chloride caused changes in expression of the largest number of genes among all biocides. In general, the four biocides tested in this study at subinhibitory concentrations did not increase the resistance potential of the pathogen to other antimicrobials. We could, however, identify clusters of genes that could possibly help the strain to grow in the presence of a biocide in the medium.
2019-12-05 | GSE135556 | GEO
Project description:Purpose: In this work, we evaluated the role of two indicative species, Citrobacter werkmanii (CW) and Escherichia albertii (EA), in the virulence of two DEC pathotypes, Shiga toxin-producing (STEC) and enteroaggregative (EAEC) Escherichia coli. Methods: To determine the effect of supernatant obtained from CW and EA cultures in STEC strain 86-24 and EAEC strain 042 gene expression, a RNA-seq analysis was performed. T84 cells were infected with DEC strains in the presence or absence of supernatant from EA and IL-8 secretion was evaluated. The effect of supernatant from EA on the growth and adherence of STEC and EAEC to T84 cells was also evaluated. Finally, we studied the participation of long polar fimbriae (Lpf) in STEC and plasmid-encoded toxin (Pet) in EAEC during DEC infection in the presence of supernatant from EA. Results: RNA-seq analysis revealed that several virulence factors in STEC and EAEC were up-regulated in the presence of supernatants from CW and EA. Interestingly, an increase in the secretion of IL-8 was observed in T84 cells infected with STEC or EAEC in the presence of a supernatant from EA. Similar results were observed with the supernatants obtained from clinical strains of E. albertii. Supernatant from EA had no effect on the growth of STEC and EAEC, or on the ability of these DEC strains to adhere to intestinal epithelial cells. Finally, we found that Pet toxin in EAEC was up-regulated in the presence of a supernatant from EA. In STEC, using mutant strains for Lpf fimbriae, our data suggested that these fimbriae might be participating in the increase of IL-8 induced by STEC on intestinal epithelial cells in the presence of a supernatant from EA. Conclusion:Supernatant obtained from an indicative species of DEC-positive diarrhea could modulate gene expression in STEC and EAEC, and IL-8 secretion induced by these bacteria. These data provide new insights into the effect of gut microbiota species in the pathogenicity of STEC and EAEC.
2022-07-22 | GSE197797 | GEO
Project description:The Salmonella effector SteC is the only protein kinase encoded by Salmonella pathogenicity island 2 that is secreted through the type III secretion system. SteC is known to trigger actin rearrangement via the phosphorylated MEK pathway, and our previous experiments demonstrated that the migration process of macrophages found during Salmonella infection is dependent on the rearrangement of the host cell actin backbone and the action of SteC.To further investigate the target of SteC in the host, we constructed a SteC-RAW264.7 cell line and performed phosphomics analysis using 4D-FastDIA to identify the direct substrates of SteC that trigger macrophage migration and lead to cytoskeletal rearrangement.
2024-02-22 | PXD042038 | Pride
Project description:Burkholderia cenocepacia is an opportunistic pathogenic bacterium intrinsically resistant to most antibiotics and biocides. The aim of this study is to map transcription start sites and 5'UTRs, and to discover novel non-coding small RNAs expressed in biofilms. The experimental approach used for this study is differential sequencing, where RNA samples are split into two aliquots, one of which is then treated with a 5' monophosphate-dependent exonuclease. Two separate libraries are created from exonuclease-treated and -untreated sub-samples, using illumina sequencing from the 5'end, without fractionation step and without depletion of abundant rRNAs. Transcription start sites can then be identified by comparing exonuclease-treated with untreated RNA-seq libraries.
2015-09-03 | E-MTAB-3381 | biostudies-arrayexpress
Project description:Shiga toxin-producing Escherichia coli (STEC) O157:H7 is a notorious foodborne pathogen capable of causing severe gastrointestinal infections in humans. The bovine rectoanal junction (RAJ) has been identified as a primary reservoir of STEC O157:H7, playing a critical role in its transmission to humans through contaminated food sources. Despite the relevance of this host-pathogen interaction, the molecular mechanisms behind the adaptation of STEC O157:H7 in the bovine RAJ and its subsequent infection of human colonic epithelial cells remain largely unexplored. This study aimed to unravel the intricate dynamics of STEC O157:H7 in two distinct host environments: bovine RAJ squamous epithelial (RSE) cells and human colonic epithelial cells. Comparative transcriptomics analysis was employed to investigate the differential gene expression profiles of STEC O157:H7 during its interaction with these cell types. The bacterial cells were cultured under controlled conditions to simulate the microenvironments of both bovine RAJ and human colonic epithelial cells. Using high-throughput RNA sequencing, we identified key bacterial genes and regulatory pathways that are significantly modulated in response to each specific host environment. Our findings reveal distinct expression patterns of virulence factors, adhesion proteins, and stress response genes in STEC O157:H7 grown in bovine RAJ cells as opposed to human colonic epithelial cells. Additionally, the comparative analysis highlights the potential role of certain genes in host adaptation and tissue-specific pathogenicity. Furthermore, this study sheds light on the potential factors contributing to the survival and persistence of STEC O157:H7 in the bovine reservoir and its ability to colonize and cause disease in humans.
2023-11-09 | GSE240423 | GEO
Project description:Study on genome-wide expression in L.monocytogenes str4b F2365 exposed to five different biocides at three different concentrations
2010-11-27 | GSE16336 | GEO
Project description:Shiga toxin-producing Escherichia coli (STEC) is a major foodborne pathogen associated with raw produce such as sprouts, where it encounters fluctuating nutrient, temperature, and oxidative stress. This study elucidated the global transcriptional adaptations of E. coli O157:H7 EDL933 during colonization and persistence on alfalfa sprouts under simulated commercial sprouting and refrigerated storage. RNA sequencing was used to compare STEC grown in tryptic soy broth (D0), colonizing fresh sprouts for 5 days (D5), and held during sprout refrigeration for additional 3 days (D8). Among 5,002 expressed genes, 782 and 826 were differentially expressed (DEGs; |log2FC| ≥ 2, adjusted p < 0.05) at D5 vs. D0, and D8 vs. D0, respectively, whereas 11 genes only differed in the D8 vs. D5 comparison, indicating that the STEC transcriptome was largely stabilized by the time sprouts reach maturity, with refrigeration inducing minimal further shifts. Transition of STEC from nutrient rich broth to sprout tissues induced a profound metabolic reprograming, characterized by the up-regulation of de novo amino acid biosynthesis (e.g., hisA–H, leuABCD, and ilv operons), to compensate for nitrogen limitation within sprout tissues. STEC further adapted to sprout environment by inducing high-affinity uptake systems for potassium (kdpA/B/C/F), phosphorus (pstSCAB), and sulfur (tauABCD), alongside enterobactin-mediated iron acquisition. To survive sprout microenvironment, STEC elevated the transcription of acid resistance (gadA/C, cadA/B), oxidative stress defense (sodA, katE/G), and envelope protection (degP, pspA–D, baeS) genes. Although initial colonization at D5 involved the induction of flagellar components, the transition to a sessile biofilm-associated lifestyle at D8 was marked by the repression of motility genes and the strong induction of curli fimbriae (csg) and colanic acid (wca) loci. Functional enrichment at D5 and D8, compared to D0, indicated coordinated stress regulation and translation. The major transcriptional trends observed in RNA seq were confirmed using RT-qPCR. Collectively, these findings highlight a multi tiered molecular adaptation strategy, enabling STEC adaptation and persistence in sprout environment, thus, providing insights that could be translated into STEC risk mitigation during sprout production
2026-05-01 | GSE329149 | GEO
Project description:Candida albicans is a commensal yeast within the human microbiota with significant medical importance because of its pathogenic potential. The yeast produces biofilms, which are highly resistant to available antifungals. High level of antifungal resistance by C. albicans biofilms has resulted in the need for alternative treatment. Polyunsaturated fatty acids such as arachidonic acid has been reported to increase the susceptibility of C. albicans biofilms to azole. However, the underlining mechanism is unknown. To unravel the mechanism behind this phenomenon, identification of differentially regulated genes in C. albicans biofilms grown in the presence of arachidonic acid, fluconazole, and the combination of both compounds was conducted using RNAseq.
2020-08-25 | GSE137423 | GEO
Project description:Antibiotic resistance is a growing concern, yet resistance and cross-resistance to widely used chemical biocides are poorly understood. Here, we show that cationic biocides induce V-type ATPase overactivation in Streptococcus gordonii, shifting metabolism to oxidative phosphorylation and increasing ROS. This triggers protein aggregation (PAs), which amplifies ROS in a lethal feedback loop. Synergistic inactivation of ClpX, a protease ATPase subunit, and PstB, a phosphate transporter component, disrupts the PAs-ROS loop by suppressing the competence regulator ComDE and rewiring metabolism to glycolysis. ClpX inactivation alleviates proteotoxic stress, promoting HtrA-mediated CSP degradation and ComDE downregulation, while PstB dysfunction impairs mannose PTS phosphorylation to further suppress ComDE. Reactivation of ComDE restores biocide susceptibility through the PAs-ROS loop. This mechanism is conserved in other ComDE-encoding streptococci, including Streptococcus pneumoniae, underscoring ComDE-mediated metabolic adaptation as a key regulator of bacterial susceptibility to membrane-targeted and ROS-inducing antimicrobials, and suggesting strategies to mitigate resistance to chemical biocides.
| PXD077459 |
Project description:Novel anti-infective agents targeting Staphylococcus aureus and capable of increasing S. aureus susceptibility towards antibiotics are needed. One alternative approach is targeting the bacterial quorum sensing (QS) system. QS is a process by which bacteria produce and detect signal molecules and thereby coordinate their behaviour, virulence and biofilm formation in a cell-density-dependent manner. Hamamelitannin (HAM) was previously suggested to target the S. aureus QS system, thereby increasing the susceptibility of S. aureus biofilms towards vancomycin. However, mechanistic insights are still lacking. For this reason, we evaluated the effect of Hamamelitannin, vancomycin and combination treatment of Hamamelitannin and vancomycin on gene expression in S. aureus Mu50 biofilms.
2017-08-25 | E-MTAB-3816 | biostudies-arrayexpress