The involvement of body appearance in influencing the biofilm formation by Escherichia coli K-12 through RodZ
Ontology highlight
ABSTRACT:
ORGANISM(S): Escherichia coli Escherichia coli str. K-12 substr. MG1655
PROVIDER: GSE63052 | GEO | 2015/11/05
SECONDARY ACCESSION(S): PRJNA266516
REPOSITORIES: GEO
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Project description:Fifty five genes were induced or reduced (2.5-fold) by the absence of rodZ genes Among them, curli production-, cell division-, and biofilm-associated genes as well as phage-related genes were regulated by the RodZ, significantly Three-condition experiment, BW25113 WT/pCA24N vs. rodZ/pCA24N vs. rodZ/pCA24N-RodZ. For preparing the total RNA, each cells were grown at 37°C upto OD600=0.5 and then keep growing with 1 mM IPTG for additional 6 h
2015-11-05 | E-GEOD-63052 | biostudies-arrayexpress
Project description:Two lineages of enterohemorrhagic (EHEC) Escherichia coli O157:H7 (EDL933, Stx1+ and Stx2+) and 86-24 (Stx2+) were investigated in regards to biofilm formation on an abiotic surface. Strikingly, EDL933 strain formed a robust biofilm while 86-24 strain formed no biofilm on either a polystyrene plate or a polyethylene tube. To identify the genetic mechanisms of different biofilm formation in two EHEC strains, DNA microarrays were first performed and phenotypic assays were followed. In the comparison of the EDL933 strain versus 86-24 strain, genes (csgBAC and csgDEFG) involved in curli biosynthesis were significantly induced while genes (trpLEDCB and mtr) involved in indole signaling were repressed. Additionally, a dozen of phage genes were differentially present between two strains. Curli assays using a Congo red plate and scanning electron microscopy corroborate the microarray data as the EDL 933 strain produces a large amount of curli, while 86-24 forms much less curli. Also, the indole production in the EDL933 was 2-times lower than that of 86-24. It was known that curli formation positively regulates and indole negatively regulates biofilm formation of EHEC. Hence, it appears that less curli formation and high indole production in the 86-24 strain are majorly responsible for no biofilm formation.
2011-01-19 | GSE19953 | GEO
Project description:Two lineages of enterohemorrhagic (EHEC) Escherichia coli O157:H7 (EDL933, Stx1+ and Stx2+) and 86-24 (Stx2+) were investigated in regards to biofilm formation on an abiotic surface. Strikingly, EDL933 strain formed a robust biofilm while 86-24 strain formed no biofilm on either a polystyrene plate or a polyethylene tube. To identify the genetic mechanisms of different biofilm formation in two EHEC strains, DNA microarrays were first performed and phenotypic assays were followed. In the comparison of the EDL933 strain versus 86-24 strain, genes (csgBAC and csgDEFG) involved in curli biosynthesis were significantly induced while genes (trpLEDCB and mtr) involved in indole signaling were repressed. Additionally, a dozen of phage genes were differentially present between two strains. Curli assays using a Congo red plate and scanning electron microscopy corroborate the microarray data as the EDL 933 strain produces a large amount of curli, while 86-24 forms much less curli. Also, the indole production in the EDL933 was 2-times lower than that of 86-24. It was known that curli formation positively regulates and indole negatively regulates biofilm formation of EHEC. Hence, it appears that less curli formation and high indole production in the 86-24 strain are majorly responsible for no biofilm formation. For the microarray experiments, E. coli O157:H7 EDL933 and 86-24 were inoculated in 25 ml of LB in 250 ml shake flasks with overnight cultures that were diluted 1:100. Cells were shaken at 250 rpm and 37°C for an absorbance of 4.0 at 600 nm. Cells were immediately chilled with dry ice and 95% ethanol (to prevent RNA degradation) for 30 sec before centrifugation in 50 ml centrifuge tubes at 13,000 g for 2 min; cell pellets were frozen immediately with dry ice and stored -80°C. RNA was isolated using Qiagen RNeasy mini Kit (Valencia, CA, USA). RNA quality was assessed by Agilent 2100 bioanalyser using the RNA 6000 Nano Chip (Agilent Technologies, Amstelveen, The Netherlands), and quantity was determined by ND-1000 Spectrophotometer (NanoDrop Technologies, Inc., DE, USA).
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2012-03-31 | GSE28193 | GEO
Project description:Honey has been widely used against bacterial infection for centuries. Previous studies suggested that honeys in high concentrations inhibited bacterial growth due to the presence of anti-microbial compounds, such as methylglyoxal, hydrogen peroxide, and peptides. In this study, we found that three honeys (acacia, clover, and polyfloral) in a low concentration as below as 0.5% (v/v) significantly suppress virulence and biofilm formation in enterohemorrhagic E. coli O157:H7 affecting the growth of planktonic cells while these honeys do not harm commensal E. coli K-12 biofilm formation. Transcriptome analyses show that honeys (0.5%) markedly repress quorum sensing genes (e.g., AI-2 import and indole biosynthesis), virulence genes (e.g., LEE genes), and curli genes (csgBAC). We found that glucose and fructose in honeys are key compounds to reduce the biofilm formation of E. coli O157:H7 via suppressing curli production, but not that of E. coli K-12. Additionally, we observed the temperature-dependent response of honeys and glucose on commensal E. coli K-12 biofilm formation; honey and glucose increase E. coli K-12 biofilm formation at 37°C, while they decrease E. coli K-12 biofilm formation at 26°C. These results suggest that honey can be a practical tool for reducing virulence and colonization of the pathogenic E. coli O157:H7, while honeys do not harm commensal E. coli community in the human. For the microarray experiments, E. coli O157:H7 EDL933 was inoculated in 250 ml of LB in 1000 ml flasks with overnight cultures that were diluted at 1:100. Cells were shaken with 10g of glass wool at 100 rpm and 37°C for 7 hrs. Cells were immediately chilled with dry ice and 95% ethanol (to prevent RNA degradation) for 30 sec before centrifugation in 50 ml centrifuge tubes at 13,000 g for 2 min; cell pellets were frozen immediately with dry ice and stored -80°C. RNA was isolated using Qiagen RNeasy mini Kit (Valencia, CA, USA). To eliminate DNA contamination, Qiagen RNase-free DNase I was used to digest DNA. RNA quality was assessed by Agilent 2100 bioanalyser using the RNA 6000 Nano Chip (Agilent Technologies, Amstelveen, The Netherlands), and quantity was determined by ND-1000 Spectrophotometer (NanoDrop Technologies, Inc., DE, USA).
2012-03-30 | E-GEOD-28193 | biostudies-arrayexpress
Project description:Pathogenic biofilms have been associated with persistent infections due to their high resistance to antimicrobial agents. To identify non-toxic biofilm inhibitors for enterohemorrhagic Escherichia coli O157:H7, indole-3-acetaldehyde was used and reduced E. coli O157:H7 biofilm formation. Global transcriptome analyses revealed that indole-3-acetaldehyde most repressed two curli operons, csgBAC and csgDEFG, and induced tryptophanase (tnaAB) in E. coli O157:H7 biofilm cells. Electron microscopy showed that indole-3-acetaldehyde reduced curli production in E. coli O157:H7. Together, this study shows that Actinomycetales are an important resource of biofilm inhibitors as well as antibiotics.
2012-07-05 | GSE30424 | GEO
Project description:Bacteriophages (hereafter “phages”) are ubiquitous predators of bacteria in the natural world, but interest is growing in their development into antibacterial therapy as complement or replacement for antibiotics. However, bacteria have evolved a huge variety of anti-phage defense systems allowing them to resist phage lysis to a greater or lesser extent, and in pathogenic bacteria these inevitably impact phage therapy outcomes. In addition to dedicated phage defense systems, some aspects of the general stress response also impact phage susceptibility, but the details of this are not well known. In order to elucidate these factors in the opportunistic pathogen Pseudomonas aeruginosa, we used the laboratory-conditioned strain PAO1 as host for phage infection experiments as it is naturally poor in dedicated phage defense systems. Screening by transposon insertion sequencing indicated that the uncharacterized operon PA3040-PA3042 was potentially associated with resistance to lytic phages. However, we found that its primary role appeared to be in regulating biofilm formation. Its expression was highly growth-phase dependent and responsive to phage infection and cell envelope stress.
2023-10-30 | GSE246284 | GEO
Project description:Intercellular signal indole and its derivative hydroxyindoles inhibit Escherichia coli biofilm and diminish Pseudomonas aeruginosa virulence. However, indole and bacterial indole derivatives were unstable in microbial community due to the widespread of diverse oxygenases that could quickly degrade them. Hence, we sought to identify novel non-toxic, stable, and potent indole derivatives from plant sources for inhibiting biofilm formation of E. coli O157:H7 and P. aeruginosa PAO1. Here, plant auxin 3-indolylacetonitrile (IAN) was found to inhibit biofilm formation of both E. coli O157:H7 and P. aeruginosa without affecting its growth. IAN inhibited biofilms more effectively than indole for both E. coli and P. aeruginosa. Additionally, IAN decreased the production of virulence factor pyocyanin in P. aeruginosa. DNA microarray analysis indicated that IAN repressed genes involved in curli formation and glycerol metabolism, while IAN induced indole-related genes and prophage genes in E. coli. It appears that IAN inhibits biofilm formation of E. coli by reducing curli formation and inducing indole production. Furthermore, unlike bacterial indole derivatives, plant-originated IAN was stable in the presence of either E. coli or P. aeruginosa.
2010-12-31 | GSE19842 | GEO
Project description:We previously discovered that yliH and yceP are induced in Escherichia coli biofilms (D. Ren, L. A. Bedzyk, S. M. Thomas, R. W. Ye, and T. K. Wood, Appl. Microbiol. Biotechnol. 64:515-524, 2004). Here, it is shown that deletion of yceP (b1060) and yliH (b0836) increases biofilm formation in continuous-flow chambers with minimal glucose medium by increasing biofilm mass (240- to 290-fold), surface coverage (16- to 31-fold), and mean thickness (2,800-fold). To determine the genetic basis of the increase in biofilm formation, we examined the differential gene expression profile in biofilms for both the mutants relative to the wild-type strain in rich medium with glucose and found that 372 to 882 genes were induced and that 76 to 337 were repressed consistently >2-fold (P < or = 0.05). The increase in biofilm formation was related to differential expression of genes related to stress response (8 to 64 genes) for both mutants, including rpoS and sdiA. More importantly, 42 to 130 genes related to autoinducer 2 cell signaling were also differentially expressed, including gadAB and flgBCEGHIJLMN, as well as signaling through indole, since 17 to 26 indole-related genes were differentially expressed, including phoAER, gltBD, mtr (encodes protein for indole import), and acrEF (encodes proteins for indole export). Increased biofilm formation in the yliH and yceP mutants in LB supplemented with 0.2% glucose (LB glu) occurred through a reduction in extracellular and intracellular indole concentrations in both mutants (50- to 140-fold), and the addition of indole to the culture restored the wild-type biofilm phenotype; hence, indole represses biofilms. Additionally, both mutants regulate biofilms through quorum sensing, since deletion of either yliH or yceP increased extracellular autoinducer 2 concentrations 50-fold when grown in complex medium (most notably in the stationary phase). Both proteins are involved in motility regulation, since YliH (127 amino acids) and YceP (84 amino acids) repressed motility two to sevenfold (P < or = 0.05) in LB, and YceP repressed motility sevenfold (P < or = 0.05) in LB glu. Heightened motility in the yceP mutant occurred, due to increased transcription of the flagella and motility loci, including fliC, motA, and qseB (3- to 86-fold). We propose new names for these two loci: bssR for yliH and bssS for yceP, based on the phrase "regulator of biofilm through signal secretion."
| S-EPMC1448992 | biostudies-literature
Project description:Pathogenic biofilms have been associated with persistent infections due to high resistance to antimicrobial agents while commensal biofilms often fortify host immune system. Hence, controlling biofilm formation of both pathogenic bacteria and commensal bacteria is important in bacteria-related diseases. We investigated the effect of plant flavonoids on biofilm formation of both enterohemorrhagic Escherichia coli O157:H7 and three commensal E. coli K-12 strains. Phloretin abundant in apples markedly reduced E. coli O157:H7 biofilm formation without affecting the growth of planktonic cells while phloretin did not harm commensal E. coli K-12 biofilms. Also, phloretin reduced E. coli O157:H7 attachment to human colon epithelial cells. Global transcriptome analyses revealed that phloretin repressed toxin genes (hlyE and stx2), autoinducer-2 importer genes (lsrACDBF), a curli gene (csgA), and a dozens of prophage genes in E. coli O157:H7 cells. Electron microscopy confirmed that phroretin reduced the curli production in E. coli O157:H7. In addition, phloretin suppressed TNF-α-induced inflammatory response in vitro using human colonic epithelial cells. Moreover, in the trinitrobenzene sulfonic acid (TNBS)-induced rat colitis model, phloretin significantly ameliorated colon inflammation and body weight loss. Taken together, our results suggest that phloretin may act as an inhibitor of E. coli O157:H7 biofilm formation as well as anti-inflammatory agent on inflammatory bowel diseases while leaving beneficial commensal E. coli biofilm intact.
2011-11-22 | GSE28144 | GEO