E. coli response to apoptotic epithelial cells [Doxo]
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ABSTRACT:
ORGANISM(S): Escherichia coli
PROVIDER: GSE244769 | GEO | 2024/08/12
REPOSITORIES: GEO
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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
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. For the microarray experiments, E. coli O157:H7 EDL933 was inoculated in 25 ml of LB in 250 ml flasks with overnight cultures that were diluted at 1:100. Cells were shaken 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).
2011-11-22 | E-GEOD-28144 | biostudies-arrayexpress
Project description:Transcriptome profiling of E. coli MG1655, E. coli EDL933, E. coli ECOR26, and E. coli Nissle 1917 grown on mouse cecal mucus as carbon source The carbon sources that support growth of pathogenic E. coli O157:H7 in the mammalian intestine have not previously been investigated. In vivo, pathogenic E. coli EDL933 primarily grows as dispersed single cells within the mucus layer that overlies the mouse cecal epithelium. We therefore compared the pathogen and commensal E. coli MG1655 for their mode of metabolism in vitro on a mixture of the sugars known to be present in cecal mucus and found that the two strains used the thirteen sugars in a similar order and co-metabolized as many as nine sugars at a time. We conducted a systematic mutational analysis of E. coli EDL933 and E. coli MG1655 with lesions in the pathways used for catabolism of thirteen mucus-derived sugars and five other compounds for which the corresponding gene system was induced in the transcriptome of cells grown on cecal mucus. Each of 18 catabolic mutants in both genetic backgrounds was fed to streptomycin-treated mice together with the respective wildtype parent strain and their colonization was monitored in fecal plate counts. None of the mutations corresponding to the five compounds not found in mucosal polysaccharides resulted in colonization defects. Based on the mutations that caused colonization defects, we determined that both E. coli EDL933 and E. coli MG1655 used arabinose, fucose, and N-acetylglucosamine in the intestine. In addition, E. coli EDL933 used galactose, hexuronates, mannose and ribose, whereas E. coli MG1655 used gluconate and N-acetylneuraminic acid. The colonization defects of six catabolic lesions were found to be additive in E. coli EDL933, but not E. coli MG1655. The data indicate that pathogenic E. coli EDL933 uses sugars that are not used by commensal E. coli MG1655 to colonize the mouse intestine. The results suggest a strategy whereby invading pathogens gain advantage by simultaneously consuming several sugars that may be available because they are not consumed by the commensal intestinal microbiota. Keywords: growth condition: carbon source was mouse cecal mucus
2008-04-25 | GSE11254 | GEO
Project description:RepA-WH1 is a synthetic bacterial prionoid, i.e., a protein that aggregates as amyloid in bacteria leading to cell death The purpose of this approach was to outline the pathways of cytotoxicity linked to RepA-WH1 expression from the set of genes induced/repressed in an Escherichia coli strain with reduced genome (MDS42)
2017-06-13 | GSE69517 | GEO
Project description:Homeostatic interactions between the host and its resident microbiota is important for normal physiological functions and if altered, it could lead to dysbiosis, a change in the structure and function of the microbiota, and as a result to various pathophysiologies. Altered structure in bacterial community is associated with various pathophysiologies, but we are just beginning to understand how these structural changes translate into functional changes. Environmental factors including pathogenic infections can lead to altered interactions between the host and its resident microbiota. We used microarray analysis and a C. elegans model system to gain insights on the mechanisms of functional changes in host-commensal bacteria interaction in the presence or absence of G. duodenalis and identified expression pattern in commensal bacteria that are characteristic of homeostatic and dysbiotic interactions. E. coli HB101 exposed to C. elegans in the presence or absence of G. duodenalis conditioned S-basal complete media for 24 hours were used for RNA extraction and hybridization on Affymetrix microarrays. We collected expression data for E. coli HB101, E. coli HB101 exposed to C. elegans, E. coli HB101 exposed to Giardia conditioned media, and E. coli HB101 exposed to both C. elegans and Giardia conditioned media.
2015-04-02 | E-GEOD-61092 | biostudies-arrayexpress
Project description:The establishment of bacterial infections at epithelial surfaces is determined by the balance of virulence attributes of the pathogen with the activity of innate host defenses. Polymorphonuclear leukocytes (PMN) are key responders in many bacterial infections, but the mechanisms by which pathogens subvert these early responses to establish infection are largely undefined. Here, we model these early interactions between human PMN and the primary cause of urinary tract infections, namely uropathogenic Escherichia coli (UPEC). Our objective was to define virulence phenotypes of uropathogens (as compared with laboratory and commensal E. coli strains) that permit evasion of PMN activity. We found that UPEC strains resist phagocytic killing and dampen the production of antimicrobial reactive oxygen species by PMNs. Analysis of the global transcriptional responses of PMN to E. coli strains revealed that UPEC exposure downregulates the expression of PMN genes involved in proinflammatory signaling and PMN chemotaxis, adhesion, and migration. Consistent with these data, UPEC attenuated transepithelial neutrophil recruitment in an in vitro model of acute infection. We propose that these UPEC strategies are important in the establishment of epithelial infection, and that the findings are germane to a range of bacterial infections at epithelial surfaces. We used microarrays to detail the global program of gene expression in human neutrophils in response to a uropathogenic bacteria compared to a closely related non-pathogenic strain relative to control samples with no bacteria. Our goal was to elucidate a pathogen-specific response. We chose an early time point of 60 minutes to evaluate the accute response to infection. Human neutrophils were exposed to pathogenic or commensal Escherichia coli for RNA extraction and hybridization on Affymetrix microarrays
2010-03-07 | E-GEOD-18810 | biostudies-arrayexpress
Project description:Escherichia coli (E. coli) amine oxidase (ECAO) encoded by tynA gene has been one of the model enzymes to study the mechanism of oxidative deamination of amines to the corresponding aldehydes by amine oxidases. The biological roles of ECAO have been less addressed. Therefore we have constructed a gene deletion Escherichia coli K-12 strain, E. coli tynA-, and used the microarray technique to address its function by comparing the total RNA gene expression to the one of the wt. Our results suggest that tynA is a reserve gene for stringent environmental conditions and its gene product ECAO a growth advantage compared to other bacteria due to H2O2 production.
2015-09-30 | GSE65385 | GEO
Project description:PhoP is considered a regulator of virulence despite being conserved in both pathogenic and non-pathogenic Enterobacteriaceae. While Escherichia coli strains represent both non-pathogenic commensal isolates and numerous virulent pathotypes, the PhoP virulence regulator has only been studied in commensal E. coli. To better understand how conserved transcription factors contribute to virulence, we characterized PhoP in pathogenic E. coli. Loss of phoP significantly attenuated E. coli during extraintestinal infection. This was not surprising since we demonstrated that PhoP differentially regulated the transcription of >600 genes. In addition to survival at acidic pH and resistance to polymyxin B, PhoP was required for repression of motility and oxygen-independent changes in the expression of primary dehydrogenase and terminal reductase respiratory chain components. All phenotypes have in common a reliance on an energized membrane. Thus, we hypothesized that PhoP mediated these effects by regulating genes that generate a proton motive force. Indeed, bacteria lacking PhoP exhibited a hyper-polarized membrane, and dissipation of the transmembrane electrochemical gradient increased the susceptibility of the phoP mutant to acidic pH, while inhibiting respiratory generation of the proton gradient restored resistance to antimicrobial peptides independent of lipopolysaccharide modification. These findings demonstrate a connection between PhoP, virulence, and the energized state of the membrane. Comparison of gene expression between wild-type CFT073 and a CFT073 phoP deletion mutant during logarithmic phase growth in LB medium. Three biological replicates were compared from each strain.
2011-07-28 | E-GEOD-31029 | biostudies-arrayexpress
Project description:Regulation of EHEC gene expression by the gut commensal bacterium B. thetaiotaomicron. EHEC is a human pathogen that colonizes in the colon where B. thetaiotaomicron is a predominant commensal. We used microarrays to evaluate global regulation of EHEC when cultured with B. thetaiotaomicron. EHEC and B. thetaiotaomicron were co-cultured in vitro under strict anaerobic conditions in low-glucose Dulbecco's modified Eagle's medium (DMEM). Total RNA from bacteria grown to mid-logarithmic phase was extracted and hybridized to an Affymetrix E. coli 2.0 gene chip according to manufacturer's specifications: http//www.affymetrix.com/support/technical/manual/expression_manual.affx
2013-05-29 | E-GEOD-47418 | biostudies-arrayexpress
Project description:Transcriptome profiling of E. coli MG1655, E. coli EDL933, E. coli ECOR26, and E. coli Nissle 1917 grown on mouse cecal mucus as carbon source The carbon sources that support growth of pathogenic E. coli O157:H7 in the mammalian intestine have not previously been investigated. In vivo, pathogenic E. coli EDL933 primarily grows as dispersed single cells within the mucus layer that overlies the mouse cecal epithelium. We therefore compared the pathogen and commensal E. coli MG1655 for their mode of metabolism in vitro on a mixture of the sugars known to be present in cecal mucus and found that the two strains used the thirteen sugars in a similar order and co-metabolized as many as nine sugars at a time. We conducted a systematic mutational analysis of E. coli EDL933 and E. coli MG1655 with lesions in the pathways used for catabolism of thirteen mucus-derived sugars and five other compounds for which the corresponding gene system was induced in the transcriptome of cells grown on cecal mucus. Each of 18 catabolic mutants in both genetic backgrounds was fed to streptomycin-treated mice together with the respective wildtype parent strain and their colonization was monitored in fecal plate counts. None of the mutations corresponding to the five compounds not found in mucosal polysaccharides resulted in colonization defects. Based on the mutations that caused colonization defects, we determined that both E. coli EDL933 and E. coli MG1655 used arabinose, fucose, and N-acetylglucosamine in the intestine. In addition, E. coli EDL933 used galactose, hexuronates, mannose and ribose, whereas E. coli MG1655 used gluconate and N-acetylneuraminic acid. The colonization defects of six catabolic lesions were found to be additive in E. coli EDL933, but not E. coli MG1655. The data indicate that pathogenic E. coli EDL933 uses sugars that are not used by commensal E. coli MG1655 to colonize the mouse intestine. The results suggest a strategy whereby invading pathogens gain advantage by simultaneously consuming several sugars that may be available because they are not consumed by the commensal intestinal microbiota. Keywords: growth condition: carbon source was mouse cecal mucus E. coli strains were grown on MOPS minimal medium containing 10 mg/ml of mucus or 0.2% glucose in 10 ml standing culture in testtubes and harvested at OD600 = 0.4.
2008-04-25 | E-GEOD-11254 | biostudies-arrayexpress