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Journal articles on the topic 'Escherichia coli Stamm Nissle 1917'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

Plaßmann, Dominik, and Hildegard Schulte-Witte. "Therapie des Reizdarmsyndroms mit Escherichia coli Stamm Nissle 1917 (EcN)." Medizinische Klinik 102, no. 11 (November 2007): 888–92. http://dx.doi.org/10.1007/s00063-007-1116-2.

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2

Altuntaş, Seda, Mihriban Korukluoğlu, and Volkan Altuntaş. "Probiotic Escherichia coli Strain Nissle 1917." Pamukkale University Journal of Engineering Sciences 23, no. 7 (2017): 933–40. http://dx.doi.org/10.5505/pajes.2017.98475.

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3

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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4

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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5

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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6

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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7

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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8

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.

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9

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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10

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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11

Yu, Xiaoli, Changsen Lin, Jing Yu, Qingsheng Qi, and Qian Wang. "Bioengineered Escherichia coli Nissle 1917 for tumour‐targeting therapy." Microbial Biotechnology 13, no. 3 (May 2020): 629–36. http://dx.doi.org/10.1111/1751-7915.13523.

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12

Grozdanov, Lubomir, Carsten Raasch, Jürgen Schulze, Ulrich Sonnenborn, Gerhard Gottschalk, Jörg Hacker, and Ulrich Dobrindt. "Analysis of the Genome Structure of the Nonpathogenic Probiotic Escherichia coli Strain Nissle 1917." Journal of Bacteriology 186, no. 16 (August 15, 2004): 5432–41. http://dx.doi.org/10.1128/jb.186.16.5432-5441.2004.

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ABSTRACT Nonpathogenic Escherichia coli strain Nissle 1917 (O6:K5:H1) is used as a probiotic agent in medicine, mainly for the treatment of various gastroenterological diseases. To gain insight on the genetic level into its properties of colonization and commensalism, this strain's genome structure has been analyzed by three approaches: (i) sequence context screening of tRNA genes as a potential indication of chromosomal integration of horizontally acquired DNA, (ii) sequence analysis of 280 kb of genomic islands (GEIs) coding for important fitness factors, and (iii) comparison of Nissle 1917 genome content with that of other E. coli strains by DNA-DNA hybridization. PCR-based screening of 324 nonpathogenic and pathogenic E. coli isolates of different origins revealed that some chromosomal regions are frequently detectable in nonpathogenic E. coli and also among extraintestinal and intestinal pathogenic strains. Many known fitness factor determinants of strain Nissle 1917 are localized on four GEIs which have been partially sequenced and analyzed. Comparison of these data with the available knowledge of the genome structure of E. coli K-12 strain MG1655 and of uropathogenic E. coli O6 strains CFT073 and 536 revealed structural similarities on the genomic level, especially between the E. coli O6 strains. The lack of defined virulence factors (i.e., alpha-hemolysin, P-fimbrial adhesins, and the semirough lipopolysaccharide phenotype) combined with the expression of fitness factors such as microcins, different iron uptake systems, adhesins, and proteases, which may support its survival and successful colonization of the human gut, most likely contributes to the probiotic character of E. coli strain Nissle 1917.

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13

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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14

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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15

Guenther, Katrin, Eberhardt Straube, Wolfgang Pfister, Albrecht Guenther, and Axel Huebler. "Sever Sepsis After Probiotic Treatment With Escherichia coli NISSLE 1917." Pediatric Infectious Disease Journal 29, no. 2 (February 2010): 188–89. http://dx.doi.org/10.1097/inf.0b013e3181c36eb9.

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16

Jo, Sung-Hyun, Han-Gyu Park, Won-Suk Song, Seong-Min Kim, Eun-Jung Kim, Yung-Hun Yang, Jae-Seok Kim, Byung-Gee Kim, and Yun-Gon Kim. "Structural characterization of phosphoethanolamine-modified lipid A from probiotic Escherichia coli strain Nissle 1917." RSC Advances 9, no. 34 (2019): 19762–71. http://dx.doi.org/10.1039/c9ra02375e.

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17

Lasaro, Melissa A., Nina Salinger, Jing Zhang, Yantao Wang, Zhengtao Zhong, Mark Goulian, and Jun Zhu. "F1C Fimbriae Play an Important Role in Biofilm Formation and Intestinal Colonization by the Escherichia coli Commensal Strain Nissle 1917." Applied and Environmental Microbiology 75, no. 1 (November 7, 2008): 246–51. http://dx.doi.org/10.1128/aem.01144-08.

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ABSTRACT Bacterial biofilm formation is thought to enhance survival in natural environments and during interaction with hosts. A robust colonizer of the human gastrointestinal tract, Escherichia coli Nissle 1917, is widely employed in probiotic therapy. In this study, we performed a genetic screen to identify genes that are involved in Nissle biofilm formation. We found that F1C fimbriae are required for biofilm formation on an inert surface. In addition, these structures are also important for adherence to epithelial cells and persistence in infant mouse colonization. The data suggest a possible connection between Nissle biofilm formation and the survival of this commensal within the host. Further study of the requirements for robust biofilm formation may improve the therapeutic efficacy of Nissle 1917.

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18

Dalziel, J. E., V. Mohan, J. Peters, R. C. Anderson, P. K. Gopal, and N. C. Roy. "The probiotic Escherichia coli Nissle 1917 inhibits propagating colonic contractions in the rat isolated large intestine." Food & Function 6, no. 1 (2015): 256–63. http://dx.doi.org/10.1039/c4fo00831f.

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Stentebjerg-Olesen, Bodil, Trinad Chakraborty, and Per Klemm. "Type 1 Fimbriation and Phase Switching in a NaturalEscherichia coli fimB Null Strain, Nissle 1917." Journal of Bacteriology 181, no. 24 (December 15, 1999): 7470–78. http://dx.doi.org/10.1128/jb.181.24.7470-7478.1999.

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ABSTRACT Escherichia coli Nissle 1917 has been used as a probiotic against intestinal disorders for many decades. It is a good colonizer of the human gut and has been reported to be able to express type 1 fimbriae. Type 1 fimbriae are surface organelles which mediate α-d-mannose-sensitive binding to various host cell surfaces. The expression is phase variable, and two tyrosine recombinases, FimB and FimE, mediate the inversion of the fimbrial phase switch. Current evidence suggests that FimB can carry out recombination in both directions, whereas FimE-catalyzed switching is on to off only. We show here that under liquid shaking growth conditions, Nissle 1917 did not express type 1 fimbriae, due to a truncation of the fimB gene by an 1,885-bp insertion element. Despite its fimB null status, Nissle 1917 was still capable of off-to-on switching of the phase switch and expressing type 1 fimbriae when grown under static conditions. This phase switching was not catalyzed by FimE, by truncated FimB, or by information residing within the insertion element. No further copies offimB seemed to be present on the chromosome of Nissle 1917, suggesting that another tyrosine recombinase in Nissle 1917 is responsible for the low-frequency off-to-on inversion of the phase switch that is strongly favored under static growth conditions. This is the first report documenting the non-FimB- or non-FimE-catalyzed inversion of the fim switch.

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20

von Buenau, R., L. Jaekel, E. Schubotz, S. Schwarz, T. Stroff, and M. Krueger. "Escherichia coli Strain Nissle 1917: Significant Reduction of Neonatal Calf Diarrhea." Journal of Dairy Science 88, no. 1 (January 2005): 317–23. http://dx.doi.org/10.3168/jds.s0022-0302(05)72690-4.

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21

Ou, Bingming, Ying Yang, Wai Liang Tham, Lin Chen, Jitao Guo, and Guoqiang Zhu. "Genetic engineering of probiotic Escherichia coli Nissle 1917 for clinical application." Applied Microbiology and Biotechnology 100, no. 20 (September 17, 2016): 8693–99. http://dx.doi.org/10.1007/s00253-016-7829-5.

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22

Leatham, Mary P., Swati Banerjee, Steven M. Autieri, Regino Mercado-Lubo, Tyrrell Conway, and Paul S. Cohen. "Precolonized Human Commensal Escherichia coli Strains Serve as a Barrier to E. coli O157:H7 Growth in the Streptomycin-Treated Mouse Intestine." Infection and Immunity 77, no. 7 (April 13, 2009): 2876–86. http://dx.doi.org/10.1128/iai.00059-09.

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ABSTRACT Different Escherichia coli strains generally have the same metabolic capacity for growth on sugars in vitro, but they appear to use different sugars in the streptomycin-treated mouse intestine (Fabich et al., Infect. Immun. 76:1143-1152, 2008). Here, mice were precolonized with any of three human commensal strains (E. coli MG1655, E. coli HS, or E. coli Nissle 1917) and 10 days later were fed 105 CFU of the same strains. While each precolonized strain nearly eliminated its isogenic strain, confirming that colonization resistance can be modeled in mice, each allowed growth of the other commensal strains to higher numbers, consistent with different commensal E. coli strains using different nutrients in the intestine. Mice were also precolonized with any of five commensal E. coli strains for 10 days and then were fed 105 CFU of E. coli EDL933, an O157:H7 pathogen. E. coli Nissle 1917 and E. coli EFC1 limited growth of E. coli EDL933 in the intestine (103 to 104 CFU/gram of feces), whereas E. coli MG1655, E. coli HS, and E. coli EFC2 allowed growth to higher numbers (106 to 107 CFU/gram of feces). Importantly, when E. coli EDL933 was fed to mice previously co-colonized with three E. coli strains (MG1655, HS, and Nissle 1917), it was eliminated from the intestine (<10 CFU/gram of feces). These results confirm that commensal E. coli strains can provide a barrier to infection and suggest that it may be possible to construct E. coli probiotic strains that prevent growth of pathogenic E. coli strains in the intestine.

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23

Krammer, H., H. Kämper, R. von Bünau, E. Zieseniß, C. Stange, F. Schlieger, I. Clever, and J. Schulze. "Probiotische Arzneimitteltherapie mit E. coli Stamm Nissle 1917 (EcN): Ergebnisse einer prospektiven Datenerhebung mit 3807 Patienten." Zeitschrift für Gastroenterologie 44, no. 08 (August 11, 2006): 651–56. http://dx.doi.org/10.1055/s-2006-926909.

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24

Li, Ruijuan, Linda Helbig, Jun Fu, Xiaoying Bian, Jennifer Herrmann, Michael Baumann, A. Francis Stewart, et al. "Expressing cytotoxic compounds in Escherichia coli Nissle 1917 for tumor-targeting therapy." Research in Microbiology 170, no. 2 (March 2019): 74–79. http://dx.doi.org/10.1016/j.resmic.2018.11.001.

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Teng, G., L. Yun, W. Ting, and W. Huahong. "P846 Elafin-expressed Escherichia coli Nissle 1917 ameliorates experimental colitis in mice." Journal of Crohn's and Colitis 13, Supplement_1 (January 25, 2019): S547. http://dx.doi.org/10.1093/ecco-jcc/jjy222.970.

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Ukena, Sya N., Anurag Singh, Ulrike Dringenberg, Regina Engelhardt, Ursula Seidler, Wiebke Hansen, André Bleich, et al. "Probiotic Escherichia coli Nissle 1917 Inhibits Leaky Gut by Enhancing Mucosal Integrity." PLoS ONE 2, no. 12 (December 12, 2007): e1308. http://dx.doi.org/10.1371/journal.pone.0001308.

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Mohsin, Mashkoor, Sebastian Guenther, Peter Schierack, Karsten Tedin, and Lothar H. Wieler. "Probiotic Escherichia coli Nissle 1917 reduces growth, Shiga toxin expression, release and thus cytotoxicity of enterohemorrhagic Escherichia coli." International Journal of Medical Microbiology 305, no. 1 (January 2015): 20–26. http://dx.doi.org/10.1016/j.ijmm.2014.10.003.

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28

Różańska, Dorota, Bożena Regulska-Ilow, Irena Choroszy-Król, and Rafał Ilow. "The role of Escherichia coli strain Nissle 1917 in the gastro-intestinal diseases." Postępy Higieny i Medycyny Doświadczalnej 68 (November 6, 2014): 1251–56. http://dx.doi.org/10.5604/17322693.1127882.

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29

Trebichavsky, Ilja, Igor Splichal, Vojtech Rada, and Alla Splichalova. "Modulation of natural immunity in the gut by Escherichia coli strain Nissle 1917." Nutrition Reviews 68, no. 8 (July 20, 2010): 459–64. http://dx.doi.org/10.1111/j.1753-4887.2010.00305.x.

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Blum-Oehler, Gabriele, Sibylle Oswald, Karin Eiteljoerge, Corinne Enders, Ulrich Sonnenborn, Wolfgang Kruis, and Joerg Hacker. "Specific detection of the probiotic Escherichia coli strain Nissle 1917 in fecal samples." Gastroenterology 124, no. 4 (April 2003): A478. http://dx.doi.org/10.1016/s0016-5085(03)82420-4.

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Graziani, C., V. Petito, F. Del Chierico, F. Mangiola, S. Pecere, E. Schiavoni, M. Pizzoferrato, et al. "P115 Escherichia coli Nissle 1917 modulate gut microbiota composition in ulcerative colitis patients." Journal of Crohn's and Colitis 11, suppl_1 (January 26, 2017): S133—S134. http://dx.doi.org/10.1093/ecco-jcc/jjx002.241.

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32

Losurdo, Giuseppe, Andrea Iannone, Antonella Contaldo, Enzo Ierardi, Alfredo Di Leo, and Mariabeatrice Principi. "Escherichia coli Nissle 1917 in Ulcerative Colitis Treatment: Systematic Review and Meta-analysis." Journal of Gastrointestinal and Liver Diseases 24, no. 4 (December 1, 2015): 499–505. http://dx.doi.org/10.15403/jgld.2014.1121.244.ecn.

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Abstract:

Background & Aims: Escherichia coli Nissle 1917 (EcN) has been recommended as a therapeutic tool for ulcerative colitis (UC) treatment. However, to date, no meta-analysis has been performed on this topic. Methods: We performed a literature search on PubMed, MEDLINE, Science Direct and EMBASE. We evaluated success rates for induction of remission, relapse rates and side effects, expressed as Intention-To-Treat. Odd ratios (OR), pooled OR and 95% confidence intervals (CI) were calculated, based on the Mantel-Haenszel method. Heterogeneity was assessed by using the χ2 and I2 statistics and, if present, a random-effects model was adopted. Results: We selected six eligible trials, with 719 patients, 390 assigned to the study group and 329 to the control group. EcN induced remission in 61.6% of cases, while in the control group (mesalazine) the remission was achieved in 69.5% of cases, with a mean difference of 7.9%. The pooled OR was 0.92 (95% CI 0.15-9.66, p=0.93). A single study showed a better performance of EcN than the placebo. A relapse of the disease occurred in 36.8% in the EcN group and in 36.1% in the control group (mesalazine), with a mean difference of 0.8%, OR=1.07, with a 95% CI of 0.70-1.64 (p=0.74). Side effects were comparable (OR=1.44, 95% CI 0.80-2.59, p=0.22). Conclusions: EcN is equivalent to mesalazine in preventing disease relapse, thus confirming current guideline recommendations. EcN seems to be as effective as controls in inducing remission and therefore, its use cannot be recommended as in one study the comparison was performed against placebo. Further studies may be helpful for this subject. Abbreviations: EcN: Escherichia coli Nissle; UC: ulcerative colitis; IBD: inflammatory bowel disease; CD: Crohn’s disease; ITT: intention-to-treat.

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Weise, Christin, Yan Zhu, Dennis Ernst, Anja A. Kühl, and Margitta Worm. "Oral administration of Escherichia coli Nissle 1917 prevents allergen-induced dermatitis in mice." Experimental Dermatology 20, no. 10 (July 11, 2011): 805–9. http://dx.doi.org/10.1111/j.1600-0625.2011.01326.x.

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Behrouzi, Ava, Hoora Mazaheri, Sarvenaz Falsafi, Zahra Hoseini Tavassol, Arfa Moshiri, and Seyed Davar Siadat. "Intestinal effect of the probiotic Escherichia coli strain Nissle 1917 and its OMV." Journal of Diabetes & Metabolic Disorders 19, no. 1 (May 1, 2020): 597–604. http://dx.doi.org/10.1007/s40200-020-00511-6.

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35

Reister, Marten, Klaus Hoffmeier, Nicolas Krezdorn, Bjoern Rotter, Chunguang Liang, Stefan Rund, Thomas Dandekar, Ulrich Sonnenborn, and Tobias A. Oelschlaeger. "Complete genome sequence of the Gram-negative probiotic Escherichia coli strain Nissle 1917." Journal of Biotechnology 187 (October 2014): 106–7. http://dx.doi.org/10.1016/j.jbiotec.2014.07.442.

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36

Yim, Jaewoo, Sung Won Cho, Beomhee Kim, Sungwoo Park, Yong Hee Han, and Sang Woo Seo. "Transcriptional Profiling of the Probiotic Escherichia coli Nissle 1917 Strain under Simulated Microgravity." International Journal of Molecular Sciences 21, no. 8 (April 11, 2020): 2666. http://dx.doi.org/10.3390/ijms21082666.

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Long-term space missions affect the gut microbiome of astronauts, especially the viability of some pathogens. Probiotics may be an effective solution for the management of gut microbiomes, but there is a lack of studies regarding the physiology of probiotics in microgravity. Here, we investigated the effects of microgravity on the probiotic Escherichia coli Nissle 1917 (EcN) by comparing transcriptomic data during exponential and stationary growth phases under simulated microgravity and normal gravity. Microgravity conditions affected several physiological features of EcN, including its growth profile, biofilm formation, stress responses, metal ion transport/utilization, and response to carbon starvation. We found that some changes, such as decreased adhesion ability and acid resistance, may be disadvantageous to EcN relative to gut pathogens under microgravity, indicating the need to develop probiotics optimized for space flight.

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Tannock, Gerald W., Ing Soo Tiong, Patricia Priest, Karen Munro, Corinda Taylor, Alice Richardson, and Michael Schultz. "Testing probiotic strain Escherichia coli Nissle 1917 (Mutaflor) for its ability to reduce carriage of multidrug-resistant E. coli by elderly residents in long-term care facilities." Journal of Medical Microbiology 60, no. 3 (March 1, 2011): 366–70. http://dx.doi.org/10.1099/jmm.0.025874-0.

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A high carriage rate of multidrug-resistant Escherichia coli (MDREC) was observed in elderly residents in long-term care facilities. A double-blinded, placebo-controlled trial was carried out to determine whether the probiotic product E. coli strain Nissle 1917 (Mutaflor) would compete with MDREC in the bowel and thereby reduce the prevalence of the multiresistant bacteria in faeces and urine. Sixty-nine patients excreting norfloxacin-resistant E. coli were randomized to probiotic or placebo groups and administered capsules twice daily. The daily dose of probiotic was 5×109–5×1010 bacteria. Faecal and urine samples were cultured at baseline and during and after the treatment period. A reduction in baseline carriage was not influenced by probiotic administration. The probiotic strain was detected in faecal specimens collected during the treatment period of only two out of 12 probiotic group subjects that were tested. Genotyping of norfloxacin-resistant E. coli isolates showed that 32 strains were prevalent among the patients. Thus, E. coli Nissle 1917 does not have the capacity to compete effectively with MDREC in the bowel of elderly patients.

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Moyle, J. R., F. Solis de los Santos, G. R. Huff, W. E. Huff, N. C. Rath, M. Farnell, A. C. Fanatico, et al. "The Probiotic Escherichia coli Nissle 1917 Enhances Early Gastrointestinal Maturation in Young Turkey Poults." International Journal of Poultry Science 11, no. 7 (June 15, 2012): 445–52. http://dx.doi.org/10.3923/ijps.2012.445.452.

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Olier, Maïwenn, Ingrid Marcq, Christel Salvador-Cartier, Thomas Secher, Ulrich Dobrindt, Michèle Boury, Valérie Bacquié, et al. "Genotoxicity of Escherichia coli Nissle 1917 strain cannot be dissociated from its probiotic activity." Gut Microbes 3, no. 6 (November 16, 2012): 501–9. http://dx.doi.org/10.4161/gmic.21737.

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Graziani, C., V. Petito, F. Del Chierico, F. Mangiola, S. Pecere, E. Schiavoni, M. Pizzoferrato, et al. "OC.14.6: Escherichia Coli Nissle 1917 Modulate GUT Microbiota Composition in Ulcerative Colitis Patients." Digestive and Liver Disease 49 (March 2017): e118-e119. http://dx.doi.org/10.1016/s1590-8658(17)30390-0.

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Massip, Clémence, Priscilla Branchu, Nadège Bossuet-Greif, Camille V. Chagneau, Déborah Gaillard, Patricia Martin, Michèle Boury, et al. "Deciphering the interplay between the genotoxic and probiotic activities of Escherichia coli Nissle 1917." PLOS Pathogens 15, no. 9 (September 23, 2019): e1008029. http://dx.doi.org/10.1371/journal.ppat.1008029.

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Goerg, Karl J., Mariola Wybierala, Jutta Rauen-Vossloh, and Claus Hader. "A new approach in pseudomembranous colitis: probiotic Escherichia coli Nissle 1917 after intestinal lavage." European Journal of Gastroenterology & Hepatology 20, no. 2 (February 2008): 155–56. http://dx.doi.org/10.1097/meg.0b013e3282f1c9be.

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43

Kotłowski, Roman. "Use of Escherichia coli Nissle 1917 producing recombinant colicins for treatment of IBD patients." Medical Hypotheses 93 (August 2016): 8–10. http://dx.doi.org/10.1016/j.mehy.2016.05.002.

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Aguilera, Laura, Lorena Toloza, Rosa Giménez, Antonia Odena, Eliandre Oliveira, Juan Aguilar, Josefa Badia, and Laura Baldomà. "Proteomic analysis of outer membrane vesicles from the probiotic strain Escherichia coli Nissle 1917." PROTEOMICS 14, no. 2-3 (January 6, 2014): 222–29. http://dx.doi.org/10.1002/pmic.201300328.

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45

Jacobi, Christoph A., and Peter Malfertheiner. "Escherichia coli Nissle 1917 (Mutaflor): New Insights into an Old Probiotic Bacterium." Digestive Diseases 29, no. 6 (2011): 600–607. http://dx.doi.org/10.1159/000333307.

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46

Barbaro, M. R., D. Fuschi, C. Cremon, M. Carapelle, P. Dino, M. M. Marcellini, G. Dothel, F. De Ponti, V. Stanghellini, and G. Barbara. "Escherichia coli Nissle 1917 restores epithelial permeability alterations induced by irritable bowel syndrome mediators." Neurogastroenterology & Motility 30, no. 8 (June 28, 2018): e13388. http://dx.doi.org/10.1111/nmo.13388.

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Brader, Peter, Jochen Stritzker, Christopher C. Riedl, Pat Zanzonico, Shangde Cai, Eva M. Burnazi, E. Rashid Ghani, et al. "Escherichia coli Nissle 1917 Facilitates Tumor Detection by Positron Emission Tomography and Optical Imaging." Clinical Cancer Research 14, no. 8 (March 27, 2008): 2295–302. http://dx.doi.org/10.1158/1078-0432.ccr-07-4254.

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Xu, Jun, Kai Xia, Pinyi Li, Chenggong Qian, Yudong Li, and Xinle Liang. "Functional investigation of the chromosomal ccdAB and hipAB operon in Escherichia coli Nissle 1917." Applied Microbiology and Biotechnology 104, no. 15 (June 13, 2020): 6731–47. http://dx.doi.org/10.1007/s00253-020-10733-6.

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He, Lian, Huijun Yang, Fei Liu, Yiyan Chen, Sijia Tang, Wei Ji, Jianli Tang, et al. "Escherichia coli Nissle 1917 engineered to express Tum-5 can restrain murine melanoma growth." Oncotarget 8, no. 49 (August 24, 2017): 85772–82. http://dx.doi.org/10.18632/oncotarget.20486.

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50

Mooren, F. C., B. H. Maleki, C. Pilat, R. Ringseis, K. Eder, M. Teschler, and K. Krüger. "Effects of Escherichia coli strain Nissle 1917 on exercise-induced disruption of gastrointestinal integrity." European Journal of Applied Physiology 120, no. 7 (May 12, 2020): 1591–99. http://dx.doi.org/10.1007/s00421-020-04382-w.

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