Academic literature on the topic 'E. coli Nissle 1917'
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Journal articles on the topic "E. coli Nissle 1917"
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Sturm, Andreas, Klaus Rilling, Daniel C. Baumgart, Konstantinos Gargas, Tay Abou-Ghazalé, Bärbel Raupach, Jana Eckert, et al. "Escherichia coli Nissle 1917 Distinctively Modulates T-Cell Cycling and Expansion via Toll-Like Receptor 2 Signaling." Infection and Immunity 73, no. 3 (March 2005): 1452–65. http://dx.doi.org/10.1128/iai.73.3.1452-1465.2005.
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ABSTRACT Although the probiotic Escherichia coli strain Nissle 1917 has been proven to be efficacious for the treatment of inflammatory bowel diseases, the underlying mechanisms of action still remain elusive. The aim of the present study was to analyze the effects of E. coli Nissle 1917 on cell cycling and apoptosis of peripheral blood and lamina propria T cells (PBT and LPT, respectively). Anti-CD3-stimulated PBT and LPT were treated with E. coli Nissle 1917-conditioned medium (E. coli Nissle 1917-CM) or heat-inactivated E. coli Nissle 1917. Cyclin B1, DNA content, and caspase 3 expression were measured by flow cytometry to assess cell cycle kinetics and apoptosis. Protein levels of several cell cycle and apoptosis modulators were determined by immunoblotting, and cytokine profiles were determined by cytometric bead array. E. coli Nissle 1917-CM inhibits cell cycling and expansion of peripheral blood but not mucosal T cells. Bacterial lipoproteins mimicked the effect of E. coli Nissle 1917-CM; in contrast, heat-inactivated E. coli Nissle 1917, lipopolysaccharide, or CpG DNA did not alter PBT cell cycling. E. coli Nissle 1917-CM decreased cyclin D2, B1, and retinoblastoma protein expression, contributing to the reduction of T-cell proliferation. E. coli Nissle 1917 significantly inhibited the expression of interleukin-2 (IL-2), tumor necrosis factor α, and gamma interferon but increased IL-10 production in PBT. Using Toll-like receptor 2 (TLR-2) knockout mice, we further demonstrate that the inhibition of PBT proliferation by E. coli Nissle 1917-CM is TLR-2 dependent. The differential reaction of circulating and tissue-bound T cells towards E. coli Nissle 1917 may explain the beneficial effect of E. coli Nissle 1917 in intestinal inflammation. E. coli Nissle 1917 may downregulate the expansion of newly recruited T cells into the mucosa and limit intestinal inflammation, while already activated tissue-bound T cells may eliminate deleterious antigens in order to maintain immunological homeostasis.
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Kamada, Nobuhiko, Kenichi Maeda, Nagamu Inoue, Tadakazu Hisamatsu, Susumu Okamoto, Kyong Su Hong, Takaya Yamada, et al. "Nonpathogenic Escherichia coli Strain Nissle 1917 Inhibits Signal Transduction in Intestinal Epithelial Cells." Infection and Immunity 76, no. 1 (October 29, 2007): 214–20. http://dx.doi.org/10.1128/iai.01193-07.
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ABSTRACT Although the probiotic Escherichia coli strain Nissle 1917 has been used for the treatment of inflammatory bowel diseases, the precise mechanisms of action of this strain remain unclear. In the present study, we estimated the anti-inflammatory effect of E. coli Nissle 1917 on inflammatory responses in vitro to determine the suppressive mechanism of Nissle 1917 on the inflammatory process. To determine the effect of E. coli Nissle 1917, the human colonic epithelial cell line HCT15 was incubated with or without E. coli Nissle 1917 or another nonpathogenic E. coli strain, K-12, and then tumor necrosis factor alpha (TNF-α)-induced interleukin-8 (IL-8) production from HCT15 cells was assessed. Enzyme-linked immunosorbent assays and real-time quantitative PCR showed that Nissle 1917 treatment suppressed TNF-α-induced IL-8 transcription and production. In addition, results from luciferase assays indicated that Nissle 1917 inhibited IL-8 promoter activity. On the other hand, these anti-inflammatory effects were not seen with E. coli K-12. In addition, heat-killed Nissle 1917 or its genomic DNA did not have this anti-inflammatory effect. Surprisingly, Nissle 1917 did not affect IL-8 transactivation pathways, such as NF-κB activation, nuclear translocation, and DNA binding, or even activation of other transcriptional factors. Furthermore, it also became evident that Nissle 1917 induced the anti-inflammatory effect without contact to epithelial cells. In conclusion, these data indicate that the nonpathogenic E. coli strain Nissle 1917 expresses a direct anti-inflammatory activity on human epithelial cells via a secreted factor which suppresses TNF-α-induced IL-8 transactivation through mechanisms different from NF-κB inhibition.
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Gronbach, Kerstin, Ute Eberle, Martina Müller, Tobias A. Ölschläger, Ulrich Dobrindt, Frank Leithäuser, Jan Hendrik Niess, et al. "Safety of Probiotic Escherichia coli Strain Nissle 1917 Depends on Intestinal Microbiota and Adaptive Immunity of the Host." Infection and Immunity 78, no. 7 (April 26, 2010): 3036–46. http://dx.doi.org/10.1128/iai.00218-10.
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ABSTRACT Probiotics are viable microorganisms that are increasingly used for treatment of a variety of diseases. Occasionally, however, probiotics may have adverse clinical effects, including septicemia. Here we examined the role of the intestinal microbiota and the adaptive immune system in preventing translocation of probiotics (e.g., Escherichia coli Nissle). We challenged C57BL/6J mice raised under germfree conditions (GF-raised C57BL/6J mice) and Rag1 −/− mice raised under germfree conditions (GF-raised Rag1 −/− mice) and under specific-pathogen-free conditions (SPF-raised Rag1 −/− mice) with probiotic E. coli strain Nissle 1917, strain Nissle 1917 mutants, the commensal strain E. coli mpk, or Bacteroides vulgatus mpk. Additionally, we reconstituted Rag1 −/− mice with CD4+ T cells. E. coli translocation and dissemination and the mortality of mice were assessed. In GF-raised Rag1 −/− mice, but not in SPF-raised Rag1 −/− mice or GF-raised C57BL/6J mice, oral challenge with E. coli strain Nissle 1917, but not oral challenge with E. coli mpk, resulted in translocation and dissemination. The mortality rate was significantly higher for E. coli strain Nissle 1917-challenged GF-raised Rag1 −/− mice (100%; P < 0.001) than for E. coli strain Nissle 1917-challenged SPF-raised Rag1 −/ − mice (0%) and GF-raised C57BL/6J mice (0%). Translocation of and mortality due to strain E. coli Nissle 1917 in GF-raised Rag1 −/− mice were prevented when mice were reconstituted with T cells prior to strain E. coli Nissle 1917 challenge, but not when mice were reconstituted with T cells after E. coli strain Nissle 1917 challenge. Cocolonization experiments revealed that E. coli mpk could not prevent translocation of strain E. coli Nissle 1917. Moreover, we demonstrated that neither lipopolysaccharide structure nor flagella play a role in E. coli strain Nissle 1917 translocation and dissemination. Our results suggest that if both the microbiota and adaptive immunity are defective, translocation across the intestinal epithelium and dissemination of the probiotic E. coli strain Nissle 1917 may occur and have potentially severe adverse effects. Future work should define the possibly related molecular factors that promote probiotic functions, fitness, and facultative pathogenicity.
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Schlee, Miriam, Jan Wehkamp, Artur Altenhoefer, Tobias A. Oelschlaeger, Eduard F. Stange, and Klaus Fellermann. "Induction of Human β-Defensin 2 by the Probiotic Escherichia coli Nissle 1917 Is Mediated through Flagellin." Infection and Immunity 75, no. 5 (February 5, 2007): 2399–407. http://dx.doi.org/10.1128/iai.01563-06.
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ABSTRACT Human β-defensin 2 (hBD-2) is an inducible antimicrobial peptide synthesized by the epithelium to counteract bacterial adherence and invasion. Proinflammatory cytokines, as well as certain bacterial strains, have been identified as potent endogenous inducers. Recently, we have found that hBD-2 induction by probiotic Escherichia coli Nissle 1917 was mediated through NF-κB- and AP-1-dependent pathways. The aim of the present study was to identify the responsible bacterial factor. E. coli Nissle 1917 culture supernatant was found to be more potent than the pellet, indicating a soluble or shed factor. Chemical analysis demonstrated the factor to be heat resistant and proteinase digestible. Several E. coli Nissle 1917 deletion mutants were constructed and tested for their ability to induce hBD-2 expression in Caco-2 cells. Deletion mutants for flagellin specifically exhibited an impaired immunostimulatory capacity. Reinsertion of the flagellin gene restored the induction capacity to normal levels. Isolated flagellin from E. coli Nissle 1917 and from Salmonella enterica serovar Enteritidis induced hBD-2 mRNA significantly in contrast to the flagellin of the apathogenic E. coli strain ATCC 25922. H1 flagellin antiserum abrogated hBD-2 expression induced by flagellin as well as E. coli Nissle 1917 supernatant, confirming that flagellin is the major stimulatory factor of E. coli Nissle 1917.
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Grabig, A., D. Paclik, C. Guzy, A. Dankof, D. C. Baumgart, J. Erckenbrecht, B. Raupach, et al. "Escherichia coli Strain Nissle 1917 Ameliorates Experimental Colitis via Toll-Like Receptor 2- and Toll-Like Receptor 4-Dependent Pathways." Infection and Immunity 74, no. 7 (July 2006): 4075–82. http://dx.doi.org/10.1128/iai.01449-05.
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ABSTRACT Toll-like receptors (TLRs) are key components of the innate immune system that trigger antimicrobial host defense responses. The aim of the present study was to analyze the effects of probiotic Escherichia coli Nissle strain 1917 in experimental colitis induced in TLR-2 and TLR-4 knockout mice. Colitis was induced in wild-type (wt), TLR-2 knockout, and TLR-4 knockout mice via administration of 5% dextran sodium sulfate (DSS). Mice were treated with either 0.9% NaCl or 107 E. coli Nissle 1917 twice daily, followed by the determination of disease activity, mucosal damage, and cytokine secretion. wt and TLR-2 knockout mice exposed to DSS developed acute colitis, whereas TLR-4 knockout mice developed significantly less inflammation. In wt mice, but not TLR-2 or TLR-4 knockout mice, E. coli Nissle 1917 ameliorated colitis and decreased proinflammatory cytokine secretion. In TLR-2 knockout mice a selective reduction of gamma interferon secretion was observed after E. coli Nissle 1917 treatment. In TLR-4 knockout mice, cytokine secretion was almost undetectable and not modulated by E. coli Nissle 1917, indicating that TLR-4 knockout mice do not develop colitis similar to the wt mice. Coculture of E. coli Nissle 1917 and human T cells increased TLR-2 and TLR-4 protein expression in T cells and increased NF-κB activity via TLR-2 and TLR-4. In conclusion, our data provide evidence that E. coli Nissle 1917 ameliorates experimental induced colitis in mice via TLR-2- and TLR-4-dependent pathways.
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Grozdanov, Lubomir, Ulrich Zähringer, Gabriele Blum-Oehler, Lore Brade, Anke Henne, Yuriy A. Knirel, Ursula Schombel, et al. "A Single Nucleotide Exchange in the wzy Gene Is Responsible for the Semirough O6 Lipopolysaccharide Phenotype and Serum Sensitivity of Escherichia coli Strain Nissle 1917." Journal of Bacteriology 184, no. 21 (November 1, 2002): 5912–25. http://dx.doi.org/10.1128/jb.184.21.5912-5925.2002.
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ABSTRACT Structural analysis of lipopolysaccharide (LPS) isolated from semirough, serum-sensitive Escherichia coli strain Nissle 1917 (DSM 6601, serotype O6:K5:H1) revealed that this strain's LPS contains a bisphosphorylated hexaacyl lipid A and a tetradecasaccharide consisting of one E. coli O6 antigen repeating unit attached to the R1-type core. Configuration of the GlcNAc glycosidic linkage between O-antigen oligosaccharide and core (β) differs from that interlinking the repeating units in the E. coli O6 antigen polysaccharide (α). The wa∗ and wb∗ gene clusters of strain Nissle 1917, required for LPS core and O6 repeating unit biosyntheses, were subcloned and sequenced. The DNA sequence of the wa∗ determinant (11.8 kb) shows 97% identity to other R1 core type-specific wa∗ gene clusters. The DNA sequence of the wb∗ gene cluster (11 kb) exhibits no homology to known DNA sequences except manC and manB. Comparison of the genetic structures of the wb∗ O6 (wb∗ from serotype O6) determinants of strain Nissle 1917 and of smooth and serum-resistant uropathogenic E. coli O6 strain 536 demonstrated that the putative open reading frame encoding the O-antigen polymerase Wzy of strain Nissle 1917 was truncated due to a point mutation. Complementation with a functional wzy copy of E. coli strain 536 confirmed that the semirough phenotype of strain Nissle 1917 is due to the nonfunctional wzy gene. Expression of a functional wzy gene in E. coli strain Nissle 1917 increased its ability to withstand antibacterial defense mechanisms of blood serum. These results underline the importance of LPS for serum resistance or sensitivity of E. coli.
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Hafez, Mohamed, Kelly Hayes, Marie Goldrick, Geoff Warhurst, Richard Grencis, and Ian S. Roberts. "The K5 Capsule of Escherichia coli Strain Nissle 1917 Is Important in Mediating Interactions with Intestinal Epithelial Cells and Chemokine Induction." Infection and Immunity 77, no. 7 (April 20, 2009): 2995–3003. http://dx.doi.org/10.1128/iai.00040-09.
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ABSTRACT Escherichia coli strain Nissle 1917 has been widely used as a probiotic for the treatment of inflammatory bowel disorders and shown to have immunomodulatory effects. Nissle 1917 expresses a K5 capsule, the expression of which often is associated with extraintestinal and urinary tract isolates of E. coli. In this paper, we investigate the role of the K5 capsule in mediating interactions between Nissle 1917 and intestinal epithelial cells. We show that the loss of capsule significantly reduced the level of monocyte chemoattractant protein 1 (MCP-1), RANTES, macrophage inflammatory protein 2α (MIP-2α), MIP-2β, interleukin-8, and gamma interferon-inducible protein 10 induction by Nissle 1917 in both Caco-2 cells and MCP-1 induction in ex vivo mouse small intestine. The complementation of the capsule-minus mutation confirmed that the effects on chemokine induction were capsule specific. The addition of purified K5, but not K1, capsular polysaccharide to the capsule-minus Nissle 1917 at least in part restored chemokine induction to wild-type levels. The purified K5 capsular polysaccharide alone was unable to stimulate chemokine production, indicating that the K5 polysaccharide was acting to mediate interactions between Nissle 1917 and intestinal epithelial cells. The induction of chemokine by Nissle 1917 was generated predominantly by interaction with the basolateral surface of Caco-2 cells, suggesting that Nissle 1917 will be most effective in inducing chemokine expression where the epithelial barrier is disrupted.
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Wehkamp, Jan, Jürgen Harder, Kai Wehkamp, Birte Wehkamp-von Meissner, Miriam Schlee, Corinne Enders, Ulrich Sonnenborn, et al. "NF-κB- and AP-1-Mediated Induction of Human Beta Defensin-2 in Intestinal Epithelial Cells by Escherichia coli Nissle 1917: a Novel Effect of a Probiotic Bacterium." Infection and Immunity 72, no. 10 (October 2004): 5750–58. http://dx.doi.org/10.1128/iai.72.10.5750-5758.2004.
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ABSTRACT Little is known about the defensive mechanisms induced in epithelial cells by pathogenic versus probiotic bacteria. The aim of our study was to compare probiotic bacterial strains such as Escherichia coli Nissle 1917 with nonprobiotic, pathogenic and nonpathogenic bacteria with respect to innate defense mechanisms in the intestinal mucosal cell. Here we report that E. coli strain Nissle 1917 and a variety of other probiotic bacteria, including lactobacilli—in contrast to more than 40 different E. coli strains tested—strongly induce the expression of the antimicrobial peptide human beta-defensin-2 (hBD-2) in Caco-2 intestinal epithelial cells in a time- and dose-dependent manner. Induction of hBD-2 through E. coli Nissle 1917 was further confirmed by activation of the hBD-2 promoter and detection of the hBD-2 peptide in the culture supernatants of E. coli Nissle 1917-treated Caco-2 cells. Luciferase gene reporter analyses and site-directed mutagenesis experiments demonstrated that functional binding sites for NF-κB and AP-1 in the hBD-2 promoter are required for induction of hBD-2 through E. coli Nissle 1917. Treatment with the NF-κB inhibitor Helenalin, as well as with SP600125, a selective inhibitor of c-Jun N-terminal kinase, blocked hBD-2 induction by E. coli Nissle 1917 in Caco-2 cells. SB 202190, a specific p38 mitogen-activated protein kinase inhibitor, and PD 98059, a selective inhibitor of extracellular signal-regulated kinase 1/2, were ineffective. This report demonstrates that probiotic bacteria may stimulate the intestinal innate defense through the upregulation of inducible antimicrobial peptides such as hBD-2. The induction of hBD-2 may contribute to an enhanced mucosal barrier to the luminal bacteria.
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Hafez, Mohamed, Kelly Hayes, Marie Goldrick, Richard K. Grencis, and Ian S. Roberts. "The K5 Capsule of Escherichia coli Strain Nissle 1917 Is Important in Stimulating Expression of Toll-Like Receptor 5, CD14, MyD88, and TRIF Together with the Induction of Interleukin-8 Expression via the Mitogen-Activated Protein Kinase Pathway in Epithelial Cells." Infection and Immunity 78, no. 5 (February 9, 2010): 2153–62. http://dx.doi.org/10.1128/iai.01406-09.
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ABSTRACT Escherichia coli strain Nissle 1917, which has been widely used as a probiotic for the treatment of inflammatory bowel disorders, expresses a K5 capsule, the expression of which is often associated with extraintestinal and urinary tract isolates of E. coli. Previously, it had been shown that the expression of a K5 capsule by Nissle 1917 was important in mediating interactions with epithelial cells and the extent of chemokine expression. In this paper, we show that infection with Nissle 1917 induces expression of Toll-like receptor 4 (TLR4) and TLR5 in Caco-2 cells and that maximal induction of TLR5 required the K5 capsule. In addition, purified K5 polysaccharide was capable of inducing expression of TLR5 and mCD14 and potentiated the activity of both TLR4 and TLR5 agonists to increase the proinflammatory response. Infection with Nissle 1917 also increased the expression of the adaptor molecules MyD88 and TRIF, which was K5 capsule dependent. By Western blot analysis, it was possible to show that induction of interleukin-8 by Nissle 1917 was predominantly through the mitogen-activated protein (MAP) kinase pathway and that expression of the K5 capsule was important for activation of the MAP kinase pathway. This paper provides new information on the function of the K5 capsule in mediating interactions between Nissle 1917 and epithelial cells and the mechanisms that underlie the probiotic properties of Nissle 1917.
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Hancock, Viktoria, Malin Dahl, and Per Klemm. "Probiotic Escherichia coli strain Nissle 1917 outcompetes intestinalpathogens during biofilm formation." Journal of Medical Microbiology 59, no. 4 (April 1, 2010): 392–99. http://dx.doi.org/10.1099/jmm.0.008672-0.
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Many bacterial infections are associated with biofilm formation. Bacterialbiofilms can develop on essentially all kinds of surfaces, producing chronicand often intractable infections. Escherichia coli is an importantpathogen causing a wide range of gastrointestinal infections. E. coli strain Nissle 1917 has been used for many decades as a probiotic againsta variety of intestinal disorders and is probably the best field-tested E. coli strain in the world. Here we have investigated the biofilm-formingcapacity of Nissle 1917. We found that the strain was a good biofilm former.Not only was it significantly better at biofilm formation than enteropathogenic,enterotoxigenic and enterohaemorrhagic E. coli strains, it was alsoable to outcompete such strains during biofilm formation. The results supportthe notion of bacterial prophylaxis employing Nissle 1917 and may partiallyexplain why the strain has a beneficial effect on many intestinal disorders.
Dissertations / Theses on the topic "E. coli Nissle 1917"
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Schmidt, Dorothea. "Molekulare Analyse des probiotischen Stamms Escherichia coli Nissle 1917." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2009. http://nbn-resolving.de/urn:nbn:de:bsz:14-ds-1243973355362-88295.
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Der probiotische Stamm E. coli Nissle 1917 ist ein Fäkalisolat, das in der Medizin traditionell zur Behandlung verschiedener gastrointestinaler Erkrankungen eingesetzt wird. Durch erfolgversprechende klinische Studien zur Remissionserhaltung bei Colitis ulcerosa, bei denen EcN als therapeutische Alternative zur Standardmedikation eingesetzt wird, ist das Interesse an den Wirkmechanismen von Probiotika stark gestiegen. EcN gehört derzeit zu den am besten untersuchten Probiotika. Einige Wirkmechanismen konnten dadurch schon aufgeklärt werden. So sind vermutlich Strukturkomponenten und stammspezifische Syntheseleistungen an der Ausprägung des probiotischen Phänotyps von EcN beteiligt. Schlüssige Konzepte, die über Gene, Genprodukte und molekulare Mechanismen den probiotischen Effekt von EcN erklären, fehlen bislang. Im Rahmen dieser Arbeit wird das Genom von EcN analysiert und auf der Basis der Genomsequenz mit anderen E. coli-Stämmen verglichen. Mit Hilfe einer Promotor-Reporter-Fusionsbibliothek (Promotorbank) werden intestinal in vivo regulierte Gene identifiziert und dadurch neue Ansätze zur Untersuchung der probiotischen Eigenschaften von EcN geschaffen. Die Grundlage für die molekulare Analyse von EcN ist die manuelle Nachannotation seines sequenzierten Genoms. Die EcN-Sequenz wird mit 13 weiteren annotierten E. coli-Sequenzen verglichen. Nach dieser Analyse kodiert EcN derzeit 121 stammspezifische Gene. Die Genomstruktur ist mit den enthaltenen genomischen Inseln und Prophagen dem Genom des uropathogenen E. coli CFT073 sehr ähnlich. Mit wenigen Ausnahmen kodiert EcN alle in E. coli CFT073 vorhandenen Virulenz- und Fitnessfaktoren, so dass auf der Nukleotidebene die nahe Verwandschaft dieser beiden Stämme bestätigt werden kann. Zudem kann gezeigt werden, dass EcN in artifiziellen Systemen wie der Zellkultur oder gnotobiotischen Mäusen ein pathogenes Potenzial hat, obgleich die Kolonisierungsfähigkeit pathogener Bakterien durch Inkubation mit EcN herabgesetzt wird. Eine wichtige Rolle bei der Besiedlung des Intestinaltrakts und der Immunstimulation von Darmepithelzellen spielt auch die globale Regulation der Genaktivität bei EcN durch den alternativen Sigma-Faktor RpoS, der im Gegensatz zu rpoS-Deletionsmutanten zu einer gesteigerten mRNA-Expression des Tight-junction Proteins ZO-1 führt. Des Weiteren führte die Untersuchung von EcN-Deletionsmutanten zu der Schlussfolgerung, dass einige genomische Inseln für Eigenschaften, die das probiotische Verhalten erklären können, eine Rolle spielen. Durch den Einsatz einer Promotorbank von EcN in konventionellen und gnotobiotischen Mäusen werden erstmalig Sequenzen von intestinal in vivo aktiven Promotoren identifiziert. Der Aufbau eines Promotor-Reportergen-Assays mit dem Biolumineszenz erzeugenden luxCDABE-Operon ermöglichte die Untersuchung ausgewählter Promotoren in vitro. Mit einem In Vivo Imaging System (IVIS) kann in weiteren Experimenten die Aktivität dieser Promotoren in lebenden Mäusen untersucht werden. Im Rahmen dieser Arbeit wird gezeigt, dass EcN kein vollkommen harmloser probiotischer Stamm ist. Weitere Informationen über EcN sind dehalb wichtig für eine optimierte Anwendung als Therapeutikum. Die molekulare Analyse ist somit eine unbedingt notwendige Grundlage für weiterführende Untersuchungen der Eigenschaften von EcN, die für seinen probiotischen Charakter verantwortlich sindThe probiotic E. coli Nissle 1917 is a fecal isolate which is traditionally used for treatment of various gastrointestinal disorders. In clinical trials where EcN was used as therapeutic alternative for remission maintenance of ulcerative colitis compared to standard medication, promising results led to an increased interest in probiotics. Today, EcN is one of the best studied probiotics. Therefore, several mechanisms of action could be enlightened. Structural components and strain-specific products are responsible for its probiotic effects. But conclusive concepts about genes, gene products and molecular mechanisms that really contribute to the probiotic character of EcN have not been offered so far. In order to create new possibilities to elucidate the probiotic traits of EcN the genome is analysed by taking this as a basis for comparison to other E. coli genomes and identification of intestinal in vivo regulated genes using a promoter-trap-library. The sequenced EcN genome is annotated and compared to 13 other so far annotated E. coli genomes. Concerning these analyses EcN encodes 121 strain-specific genes. The genome structure including the genomic islands and prophages is highly homolog to the uropathogenic E. coli CFT073. EcN encodes most of the virulence and fitness factors that are present in E. coli CFT073. Therefore, the close relationship of these two strains is confirmed at nucleotide level. Furthermore, it is shown that in artificial systems like cell culture assays and gnotobiotic mice EcN reveals a pathogenic potential although EcN is able to decrease colonization efficiency of pathogenic bacteria. The alternative sigma factor RpoS that is responsible for global regulation and activity of several genes seems to play an important role during colonization of EcN in the intestine and its immunostimulatory effects on intestinal epithelial cells. Investigation of EcN-deletion mutants lacking genomic islands and prophages lead to the conclusion that some genomic islands may play a role for specific probiotic traits. This is the first time where a promoter-trap-library was used in conventional and gnotobiotic mice for collection of intestinal in vivo active promoters. Constructing and establishing a promoter-reporter gene assay with the bioluminescent luxCDABE operon made the investigation of selected promoters in vitro possible as well as establishing a bioluminescence assay using an In Vivo Imaging System (IVIS) for investigation of promoter activity in living mice. In this research project was shown that EcN is not a completely harmless probiotic. The genome structure and regulatory mechanisms of gene expression are the strain’s molecular traits that lead to probiotic activity and immunostimulatory effects. Therefore, the molecular analyses presented here, together with the complete genome sequence, are a basis for further investigations of mechanisms that are responsible for the probiotic effects of EcN
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Ozdemir, Tanel. "Design and construction of therapeutic bacterial sensors in Escherichia coli Nissle 1917." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10044236/.
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The human microbiota refers to the ecosystem of microorganisms living on or within the human body, and is increasingly being implicated as a regulator of health and disease. Abnormal alterations in the development or composition of the intestinal microbiota are referred to as dysbiosis. However, the reciprocal interactions between the microbiota and the host’s diet, immunology and genetics can in turn make it extremely difficult to distinguish the cause and effect of dysbiosis in pathologies. Synthetic biology has facilitated the design and creation of more complex and clinically relevant genetic circuits. The commensal nature of the intestinal microbiota and its constituents provide a number of well tolerated microorganisms such as Escherichia coli NISSLE 1917 (EcN) that could be used as powerful investigative tools. The use of antibiotic selection within synthetic circuits would eventually hinder their investigative power during microbiota experiments. Toxin-Antitoxin (TA) post segregational killing systems are a naturally occurring bacterial mechanism to maintain plasmid stability. Here we show that the Axe/Txe TA system from Enterococcus faecium was able to significantly outperform the more widely used Hok/Sok system to maintain the stability of fluorescent and luminescent reporter plasmids in EcN without antibiotic selection during both liquid culture and in vivo animal experiments. In addition, we created a sensor circuit that in EcN could detect both exogenous and bacterial-derived reactive nitrogen species, which are thought to play a crucial role in the human host inflammatory response. We also developed biosensors for pH and the short-chain fatty acid propionate. Finally, we demonstrated that an EcN sensor could detect and report on environmental signals in vivo from the intestines of the Caenorhabditis elegans worm. Synthetic biological tools such as these could help further elucidate the underlying role of the microbiota in conditions such as inflammatory bowel disease and cancers of the gasterointestinal tract.
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Nzakizwanayo, Jonathan. "Investigation of host-microbe interactions in the probiotic bacteria Escherichia coli Nissle 1917." Thesis, University of Brighton, 2014. https://research.brighton.ac.uk/en/studentTheses/feb9d228-0d2d-4710-9ce6-3abfcb5a3f1f.
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Probiotics are generally live preparations of bacteria that exert beneficial effects on host health when ingested in sufficient quantities. The novel probiotic Escherichia coli strain Nissle 1917 (EcN) has been shown to have a number of beneficial effects in this context, including protection against food-borne pathogens and infectious diarrheal diseases, and maintaining remission of inflammatory bowel diseases by virtue of its anti-inflammatory properties. However, little is known regarding the mechanisms underlying the beneficial effects of this organism. The overall aim of this work was to provide a greater understanding of the mechanisms through which EcN interacts with the mammalian gastro-intestinal epithelium to benefit human health.
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Troschke, Ilka [Verfasser]. "Signaltransduktion und Signalverarbeitung des probiotischen Bakteriums E. coli Nissle 1917 in vitro / Ilka Troschke." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1022761323/34.
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Berg, Jennifer [Verfasser]. "Klinischer Einsatz und Immunmodulation durch apathogene Escherichia coli Nissle 1917 bei Gräserpollenallergikern / Jennifer Berg." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1032558512/34.
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Rilling, Klaus. "Beeinflussung der Apoptoserate und Zellzyklusprogression humaner T-Zellen durch den probiotischen E. coli Stamm Nissle 1917." Doctoral thesis, [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=978696336.
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Blümlein, Ulrike [Verfasser]. "Infektionsprophylaxe mit Escherichia coli Stamm Nissle 1917 bei Frühgeborenen unter 1500 g : eine Pilotstudie / Ulrike Blümlein." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/1030056331/34.
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Vattakaven, Thomas. "Investigation of the probiotic effects of Escherichia coli Nissle 1917 using whole cell bioluminescent bacterial biosensors." Thesis, University of the West of England, Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.524724.
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Gratz, Brigitte Antonia. "Anwendung von probiotischen Escherichia coli Stamm Nissle 1917 zur Therapie gastrointestinaler Dysregulationen mit der Leitsymptomatik Diarrhöe beim Hund." Berlin Mensch-&-Buch-Verl, 2009. http://d-nb.info/1000782255/04.
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Kassem, Sahar. "Rôle du gène Vav1 et du probiotique Escherichia coli Nissle 1917 dans la susceptibilité à l'inflammation du système nerveux central." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30235.
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La Sclérose en Plaques (SEP) est une maladie d'origine multifactorielle qui se développe chez des individus génétiquement susceptibles en présence de facteurs environnementaux inducteurs. Ma thèse avait pour objectif d'analyser les effets d'un facteur génétique, le variant R63W du gène Vav1 et d'un facteur environnemental, la souche "Escherichia coli Nissle 1917", sur le développement de l'encéphalomyélite auto-immune expérimentale (EAE), un modèle animal de la SEP. Une région de 1cM comportant un polymorphisme dans le gène Vav1 a en effet été identifiée au laboratoire comme étant responsable de la résistance des rats Brown-Norway à l'EAE. Afin d'établir formellement le rôle de ce polymorphisme dans ce modèle, une souris Knock-In Vav1R63W a été générée. Nous avons montré que les souris Vav1R63W développent une EAE moins sévère. Ceci est associé à un défaut de production de cytokines inflammatoires intrinsèque aux lymphocytes T (LT) CD4 qui n'est pas lié à une augmentation de la fréquence de LT régulateurs. Sur le plan moléculaire, Vav1R63W présente une activité adaptatrice défectueuse conduisant à la diminution de la phosphorylation de ERK, AKT et p38 mais à une activité enzymatique normale. Nos résultats montrent un rôle de la fonction adaptatrice de Vav1 dans les fonctions des LT CD4 et son implication dans la susceptibilité à l'inflammation du système nerveux central (SNC). L'analyse de l'effet d'un traitement oral par le probiotique E. coli Nissle 1917 (ECN) montre un effet bénéfique sur le développement de l'EAE. Ceci est associé à un défaut de la sécrétion de cytokines par les LT CD4, ainsi qu'à une diminution de l'infiltration de LT CD4 auto-réactifs dans le SNC. De plus, la barrière intestinale est moins altérée chez les souris traitées par ECN au cours du développement de l'EAE. L'effet bénéfique de ECN semble être dû à la production d'une génotoxine, la colibactine. Par contre, la colonisation néonatale des souris C57BL/6 par ECN ne reproduit pas le même effet observé à l'âge adulte. Dans l'ensemble, nos résultats montrent un effet bénéfique du changement de la fonction de Vav1 ainsi que du traitement par ECN sur le développement de l'EAE. L'analyse approfondie des mécanismes mis en jeu, permettra une meilleure compréhension de la pathogenèse de la SEP et pourrait contribuer à l'identification de nouvelles options thérapeutiquesMultiple sclerosis (MS) is a demyelinating disease of the central nervous system. It develops in genetically susceptible individuals when they encounter specific environmental factors. The aim of my thesis was to analyze the role of a genetic factor (Vav1R63W variant) and an environmental factor (Escherichia coli Nissle 1917) in the development of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Previous genetic studies of my team suggest the implication of a polymorphism in the Vav1 gene in the resistance of Brown-Norway rats to EAE. In order to analyze the role of the identified polymorphism in the susceptibility to EAE, we generated a Knock-In mouse bearing the same polymorphism (Vav1R63W). Using this model, we showed that Vav1R63W mice develop less severe EAE due to a defect in cytokine production by CD4 T cells. This defect is intrinsic to CD4 T cells and is not linked to the increased proportion of regulatory T cells observed in Vav1R63W mice. We also showed that Vav1R63W present an altered adaptor function as shown by reduced ERK and AKT phosphorylation and decreased calcium flux after TCR stimulation, with no effect on Vav1 enzymatic activity. Thus, our results highlight the role of Vav1 adaptor function in CD4 T cell functions and susceptibility to central nervous system inflammation. Next, I analyzed the impact of the treatment with the probiotic E. coli Nissle 1917 (ECN) on EAE development. Our results showed that the daily oral treatment of adult C57BL/6 mice with ECN ameliorates the course of the disease. In addition to their defect in cytokines production, MOG specific CD4 T cells from ECN treated mice were increased in the periphery. Consequently, ECN treated mice exhibited reduced CD4 T cell infiltration in their central nervous system. Furthermore, analysis of intestinal permeability revealed that its alteration after MOG immunization was partially reversed after ECN treatment. The reduced EAE seems to be due to the secretion of a genotoxin by ECN, the colibactin. In contrast, neonatal colonization of C57BL/6 mice did not protect against EAE. Together, our data showed a beneficial role of the imbalance of Vav1 function and ECN treatment in EAE development. Further analysis of the involved mechanisms will help us to better understand the pathogenesis of MS and to develop new therapeutic strategies for MS
Book chapters on the topic "E. coli Nissle 1917"
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Schultz, M., and J. P. Burton. "Escherichia coli Nissle 1917." In The Microbiota in Gastrointestinal Pathophysiology, 59–69. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-804024-9.00005-7.
Full textConference papers on the topic "E. coli Nissle 1917"
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Ozdemir, T., A. Fedorec, and C. Barnes. "Toxin-Antitoxin Stabilised Biosensors in the Commensal Escherichia coli Nissle 1917 for the Detection of Dysbiotic Changes in the Intestinal Microbiota." In IET/SynbiCITE Engineering Biology Conference. Institution of Engineering and Technology, 2016. http://dx.doi.org/10.1049/cp.2016.1242.
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