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Gad Frankel - One of the best experts on this subject based on the ideXlab platform.

  • Citrobacter Rodentium–host–microbiota interactions: immunity, bioenergetics and metabolism
    Nature Reviews Microbiology, 2019
    Co-Authors: Caroline Mullineaux-sanders, Julia Sanchez-garrido, Eve G. D. Hopkins, Avinash R. Shenoy, Rachael Barry, Gad Frankel
    Abstract:

    Citrobacter Rodentium , an extracellular mouse-specific enteric pathogen, provides a robust model for the study of physiological host–pathogen–microbiota interactions. In this Review, Frankel and colleagues highlight how the C. Rodentium model has advanced our understanding of enteric infections and inflammatory bowel disease, in particular changes to host metabolism and inflammation. Citrobacter Rodentium is an extracellular enteric mouse-specific pathogen used to model infections with human pathogenic Escherichia coli and inflammatory bowel disease. C. Rodentium injects type III secretion system effectors into intestinal epithelial cells (IECs) to target inflammatory, metabolic and cell survival pathways and establish infection. While the host responds to infection by activating innate and adaptive immune signalling, required for clearance, the IECs respond by rapidly shifting bioenergetics to aerobic glycolysis, which leads to oxygenation of the epithelium, an instant expansion of mucosal-associated commensal Enterobacteriaceae and a decline of obligate anaerobes. Moreover, infected IECs reprogramme intracellular metabolic pathways, characterized by simultaneous activation of cholesterol biogenesis, import and efflux, leading to increased serum and faecal cholesterol levels. In this Review we summarize recent advances highlighting the intimate relationship between C. Rodentium pathogenesis, metabolism and the gut microbiota.

  • Citrobacter Rodentium-host-microbiota interactions: immunity, bioenergetics and metabolism.
    Nature Reviews Microbiology, 2019
    Co-Authors: Caroline Mullineaux-sanders, Julia Sanchez-garrido, Eve G. D. Hopkins, Avinash R. Shenoy, Rachael Barry, Gad Frankel
    Abstract:

    Citrobacter Rodentium is an extracellular enteric mouse-specific pathogen used to model infections with human pathogenic Escherichia coli and inflammatory bowel disease. C. Rodentium injects type III secretion system effectors into intestinal epithelial cells (IECs) to target inflammatory, metabolic and cell survival pathways and establish infection. While the host responds to infection by activating innate and adaptive immune signalling, required for clearance, the IECs respond by rapidly shifting bioenergetics to aerobic glycolysis, which leads to oxygenation of the epithelium, an instant expansion of mucosal-associated commensal Enterobacteriaceae and a decline of obligate anaerobes. Moreover, infected IECs reprogramme intracellular metabolic pathways, characterized by simultaneous activation of cholesterol biogenesis, import and efflux, leading to increased serum and faecal cholesterol levels. In this Review we summarize recent advances highlighting the intimate relationship between C. Rodentium pathogenesis, metabolism and the gut microbiota. Citrobacter Rodentium, an extracellular mouse-specific enteric pathogen, provides a robust model for the study of physiological host–pathogen–microbiota interactions. In this Review, Frankel and colleagues highlight how the C. Rodentium model has advanced our understanding of enteric infections and inflammatory bowel disease, in particular changes to host metabolism and inflammation.

  • Citrobacter Rodentium mouse model of bacterial infection
    Nature Protocols, 2016
    Co-Authors: Valerie F Crepin, James W Collins, Maryam Habibzay, Gad Frankel
    Abstract:

    Infection of mice with Citrobacter Rodentium is a robust model to study bacterial pathogenesis, mucosal immunology, the health benefits of probiotics and the role of the microbiota during infection. C. Rodentium was first isolated by Barthold from an outbreak of mouse diarrhea in Yale University in 1972 and was 'rediscovered' by Falkow and Schauer in 1993. Since then the use of the model has proliferated, and it is now the gold standard for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively). Here we provide a detailed protocol for various applications of the model, including bacterial growth, site-directed mutagenesis, mouse inoculation (from cultured cells and after cohabitation), monitoring of bacterial colonization, tissue extraction and analysis, immune responses, probiotic treatment and microbiota analysis. The main protocol, from mouse infection to clearance and analysis of tissues and host responses, takes ∼5 weeks to complete. Infection of mice with Citrobacter Rodentium is the gold-standard method for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli . This protocol details the use of this important mouse model of bacterial infection.

  • Citrobacter Rodentium mouse model of bacterial infection
    Nature Protocols, 2016
    Co-Authors: Valerie F Crepin, James W Collins, Maryam Habibzay, Gad Frankel
    Abstract:

    Infection of mice with Citrobacter Rodentium is a robust model to study bacterial pathogenesis, mucosal immunology, the health benefits of probiotics and the role of the microbiota during infection. C. Rodentium was first isolated by Barthold from an outbreak of mouse diarrhea in Yale University in 1972 and was 'rediscovered' by Falkow and Schauer in 1993. Since then the use of the model has proliferated, and it is now the gold standard for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively). Here we provide a detailed protocol for various applications of the model, including bacterial growth, site-directed mutagenesis, mouse inoculation (from cultured cells and after cohabitation), monitoring of bacterial colonization, tissue extraction and analysis, immune responses, probiotic treatment and microbiota analysis. The main protocol, from mouse infection to clearance and analysis of tissues and host responses, takes ∼5 weeks to complete.

  • fermented dairy products modulate Citrobacter Rodentium induced colonic hyperplasia
    The Journal of Infectious Diseases, 2014
    Co-Authors: James W Collins, Valerie F Crepin, Christian Chervaux, Benoit Raymond, Muriel Derrien, Rémi Brazeilles, Artemis Kosta, Isabelle Chambaud, Gad Frankel
    Abstract:

    We evaluated the protective effects of fermented dairy products (FDPs) in an infection model, using the mouse pathogen Citrobacter Rodentium (CR). Treatment of mice with FDP formulas A, B, and C or a control product did not affect CR colonization, organ specificity, or attaching and effacing lesion formation. Fermented dairy product A (FDP-A), but neither the supernatant from FDP-A nor β-irradiated (IR) FDP-A, caused a significant reduction in colonic crypt hyperplasia and CR-associated pathology. Profiling the gut microbiota revealed that IR-FDP-A promoted higher levels of phylotypes belonging to Alcaligenaceae and a decrease in Lachnospiraceae (Ruminococcus) during CR infection. Conversely, FDP-A prevented a decrease in Ruminococcus and increased Turicibacteraceae (Turicibacter). Importantly, loss of Ruminococcus and Turicibacter has been associated with susceptibility to dextran sodium sulfate–induced colitis. Our results demonstrate that viable bacteria in FDP-A reduced CR-induced colonic crypt hyperplasia and prevented the loss of key bacterial genera that may contribute to disease pathology.

Valerie F Crepin - One of the best experts on this subject based on the ideXlab platform.

  • Citrobacter Rodentium Relies on Commensals for Colonization of the Colonic Mucosa.
    Cell Reports, 2017
    Co-Authors: Caroline Mullineaux-sanders, James W Collins, David Ruano-gallego, Maayan Levy, Meirav Pevsner-fischer, Izabela Glegola-madejska, Agnes M. Sågfors, Joshua L.c. Wong, Eran Elinav, Valerie F Crepin
    Abstract:

    We investigated the role of commensals at the peak of infection with the colonic mouse pathogen Citrobacter Rodentium. Bioluminescent and kanamycin (Kan)-resistant C. Rodentium persisted avirulently in the cecal lumen of mice continuously treated with Kan. A single Kan treatment was sufficient to displace C. Rodentium from the colonic mucosa, a phenomenon not observed following treatment with vancomycin (Van) or metronidazole (Met). Kan, Van, and Met induce distinct dysbiosis, suggesting C. Rodentium relies on specific commensals for colonic colonization. Expression of the master virulence regulator ler is induced in germ-free mice, yet C. Rodentium is only seen in the cecal lumen. Moreover, in conventional mice, a single Kan treatment was sufficient to displace C. Rodentium constitutively expressing Ler from the colonic mucosa. These results show that expression of virulence genes is not sufficient for colonization of the colonic mucosa and that commensals are essential for a physiological infection course.

  • Citrobacter Rodentium Subverts ATP Flux and Cholesterol Homeostasis in Intestinal Epithelial Cells In Vivo.
    Cell Metabolism, 2017
    Co-Authors: Cedric N. Berger, Gordon Dougan, Valerie F Crepin, Meirav Pevsner-fischer, Theodoros I. Roumeliotis, James C. Wright, Danielle Carson, R. Christopher D. Furniss, Mally Dori-bachash
    Abstract:

    The intestinal epithelial cells (IECs) that line the gut form a robust line of defense against ingested pathogens. We investigated the impact of infection with the enteric pathogen Citrobacter Rodentium on mouse IEC metabolism using global proteomic and targeted metabolomics and lipidomics. The major signatures of the infection were upregulation of the sugar transporter Sglt4, aerobic glycolysis, and production of phosphocreatine, which mobilizes cytosolic energy. In contrast, biogenesis of mitochondrial cardiolipins, essential for ATP production, was inhibited, which coincided with increased levels of mucosal O2 and a reduction in colon-associated anaerobic commensals. In addition, IECs responded to infection by activating Srebp2 and the cholesterol biosynthetic pathway. Unexpectedly, infected IECs also upregulated the cholesterol efflux proteins AbcA1, AbcG8, and ApoA1, resulting in higher levels of fecal cholesterol and a bloom of Proteobacteria. These results suggest that C. Rodentium manipulates host metabolism to evade innate immune responses and establish a favorable gut ecosystem.

  • Citrobacter Rodentium mouse model of bacterial infection
    Nature Protocols, 2016
    Co-Authors: Valerie F Crepin, James W Collins, Maryam Habibzay, Gad Frankel
    Abstract:

    Infection of mice with Citrobacter Rodentium is a robust model to study bacterial pathogenesis, mucosal immunology, the health benefits of probiotics and the role of the microbiota during infection. C. Rodentium was first isolated by Barthold from an outbreak of mouse diarrhea in Yale University in 1972 and was 'rediscovered' by Falkow and Schauer in 1993. Since then the use of the model has proliferated, and it is now the gold standard for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively). Here we provide a detailed protocol for various applications of the model, including bacterial growth, site-directed mutagenesis, mouse inoculation (from cultured cells and after cohabitation), monitoring of bacterial colonization, tissue extraction and analysis, immune responses, probiotic treatment and microbiota analysis. The main protocol, from mouse infection to clearance and analysis of tissues and host responses, takes ∼5 weeks to complete. Infection of mice with Citrobacter Rodentium is the gold-standard method for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli . This protocol details the use of this important mouse model of bacterial infection.

  • Citrobacter Rodentium mouse model of bacterial infection
    Nature Protocols, 2016
    Co-Authors: Valerie F Crepin, James W Collins, Maryam Habibzay, Gad Frankel
    Abstract:

    Infection of mice with Citrobacter Rodentium is a robust model to study bacterial pathogenesis, mucosal immunology, the health benefits of probiotics and the role of the microbiota during infection. C. Rodentium was first isolated by Barthold from an outbreak of mouse diarrhea in Yale University in 1972 and was 'rediscovered' by Falkow and Schauer in 1993. Since then the use of the model has proliferated, and it is now the gold standard for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively). Here we provide a detailed protocol for various applications of the model, including bacterial growth, site-directed mutagenesis, mouse inoculation (from cultured cells and after cohabitation), monitoring of bacterial colonization, tissue extraction and analysis, immune responses, probiotic treatment and microbiota analysis. The main protocol, from mouse infection to clearance and analysis of tissues and host responses, takes ∼5 weeks to complete.

  • fermented dairy products modulate Citrobacter Rodentium induced colonic hyperplasia
    The Journal of Infectious Diseases, 2014
    Co-Authors: James W Collins, Valerie F Crepin, Christian Chervaux, Benoit Raymond, Muriel Derrien, Rémi Brazeilles, Artemis Kosta, Isabelle Chambaud, Gad Frankel
    Abstract:

    We evaluated the protective effects of fermented dairy products (FDPs) in an infection model, using the mouse pathogen Citrobacter Rodentium (CR). Treatment of mice with FDP formulas A, B, and C or a control product did not affect CR colonization, organ specificity, or attaching and effacing lesion formation. Fermented dairy product A (FDP-A), but neither the supernatant from FDP-A nor β-irradiated (IR) FDP-A, caused a significant reduction in colonic crypt hyperplasia and CR-associated pathology. Profiling the gut microbiota revealed that IR-FDP-A promoted higher levels of phylotypes belonging to Alcaligenaceae and a decrease in Lachnospiraceae (Ruminococcus) during CR infection. Conversely, FDP-A prevented a decrease in Ruminococcus and increased Turicibacteraceae (Turicibacter). Importantly, loss of Ruminococcus and Turicibacter has been associated with susceptibility to dextran sodium sulfate–induced colitis. Our results demonstrate that viable bacteria in FDP-A reduced CR-induced colonic crypt hyperplasia and prevented the loss of key bacterial genera that may contribute to disease pathology.

James W Collins - One of the best experts on this subject based on the ideXlab platform.

  • Citrobacter Rodentium Relies on Commensals for Colonization of the Colonic Mucosa.
    Cell Reports, 2017
    Co-Authors: Caroline Mullineaux-sanders, James W Collins, David Ruano-gallego, Maayan Levy, Meirav Pevsner-fischer, Izabela Glegola-madejska, Agnes M. Sågfors, Joshua L.c. Wong, Eran Elinav, Valerie F Crepin
    Abstract:

    We investigated the role of commensals at the peak of infection with the colonic mouse pathogen Citrobacter Rodentium. Bioluminescent and kanamycin (Kan)-resistant C. Rodentium persisted avirulently in the cecal lumen of mice continuously treated with Kan. A single Kan treatment was sufficient to displace C. Rodentium from the colonic mucosa, a phenomenon not observed following treatment with vancomycin (Van) or metronidazole (Met). Kan, Van, and Met induce distinct dysbiosis, suggesting C. Rodentium relies on specific commensals for colonic colonization. Expression of the master virulence regulator ler is induced in germ-free mice, yet C. Rodentium is only seen in the cecal lumen. Moreover, in conventional mice, a single Kan treatment was sufficient to displace C. Rodentium constitutively expressing Ler from the colonic mucosa. These results show that expression of virulence genes is not sufficient for colonization of the colonic mucosa and that commensals are essential for a physiological infection course.

  • Citrobacter Rodentium mouse model of bacterial infection
    Nature Protocols, 2016
    Co-Authors: Valerie F Crepin, James W Collins, Maryam Habibzay, Gad Frankel
    Abstract:

    Infection of mice with Citrobacter Rodentium is a robust model to study bacterial pathogenesis, mucosal immunology, the health benefits of probiotics and the role of the microbiota during infection. C. Rodentium was first isolated by Barthold from an outbreak of mouse diarrhea in Yale University in 1972 and was 'rediscovered' by Falkow and Schauer in 1993. Since then the use of the model has proliferated, and it is now the gold standard for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively). Here we provide a detailed protocol for various applications of the model, including bacterial growth, site-directed mutagenesis, mouse inoculation (from cultured cells and after cohabitation), monitoring of bacterial colonization, tissue extraction and analysis, immune responses, probiotic treatment and microbiota analysis. The main protocol, from mouse infection to clearance and analysis of tissues and host responses, takes ∼5 weeks to complete. Infection of mice with Citrobacter Rodentium is the gold-standard method for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli . This protocol details the use of this important mouse model of bacterial infection.

  • Citrobacter Rodentium mouse model of bacterial infection
    Nature Protocols, 2016
    Co-Authors: Valerie F Crepin, James W Collins, Maryam Habibzay, Gad Frankel
    Abstract:

    Infection of mice with Citrobacter Rodentium is a robust model to study bacterial pathogenesis, mucosal immunology, the health benefits of probiotics and the role of the microbiota during infection. C. Rodentium was first isolated by Barthold from an outbreak of mouse diarrhea in Yale University in 1972 and was 'rediscovered' by Falkow and Schauer in 1993. Since then the use of the model has proliferated, and it is now the gold standard for studying virulence of the closely related human pathogens enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively). Here we provide a detailed protocol for various applications of the model, including bacterial growth, site-directed mutagenesis, mouse inoculation (from cultured cells and after cohabitation), monitoring of bacterial colonization, tissue extraction and analysis, immune responses, probiotic treatment and microbiota analysis. The main protocol, from mouse infection to clearance and analysis of tissues and host responses, takes ∼5 weeks to complete.

  • fermented dairy products modulate Citrobacter Rodentium induced colonic hyperplasia
    The Journal of Infectious Diseases, 2014
    Co-Authors: James W Collins, Valerie F Crepin, Christian Chervaux, Benoit Raymond, Muriel Derrien, Rémi Brazeilles, Artemis Kosta, Isabelle Chambaud, Gad Frankel
    Abstract:

    We evaluated the protective effects of fermented dairy products (FDPs) in an infection model, using the mouse pathogen Citrobacter Rodentium (CR). Treatment of mice with FDP formulas A, B, and C or a control product did not affect CR colonization, organ specificity, or attaching and effacing lesion formation. Fermented dairy product A (FDP-A), but neither the supernatant from FDP-A nor β-irradiated (IR) FDP-A, caused a significant reduction in colonic crypt hyperplasia and CR-associated pathology. Profiling the gut microbiota revealed that IR-FDP-A promoted higher levels of phylotypes belonging to Alcaligenaceae and a decrease in Lachnospiraceae (Ruminococcus) during CR infection. Conversely, FDP-A prevented a decrease in Ruminococcus and increased Turicibacteraceae (Turicibacter). Importantly, loss of Ruminococcus and Turicibacter has been associated with susceptibility to dextran sodium sulfate–induced colitis. Our results demonstrate that viable bacteria in FDP-A reduced CR-induced colonic crypt hyperplasia and prevented the loss of key bacterial genera that may contribute to disease pathology.

  • Citrobacter Rodentium: infection, inflammation and the microbiota
    Nature Reviews Microbiology, 2014
    Co-Authors: James W Collins, Valerie F Crepin, Kristie M. Keeney, Vijay A. K. Rathinam, Katherine A. Fitzgerald, B. Brett Finlay, Gad Frankel
    Abstract:

    The mouse pathogen Citrobacter Rodentium is a useful model to investigate important human intestinal diseases, including enteropathogenic Escherichia coli (EPEC) and enterohaemorrhagic E. coli (EHEC) infections, Crohn's disease, ulcerative colitis and colon tumorigenesis. Whole-genome sequencing of multiple pathogenic attaching and effacing (A/E) bacteria has led to the identification of many genes that are involved in pathogenesis, including gene families that encode effector proteins of the type III secretion system (T3SS). The functions of many putative virulence genes have been evaluated in the C. Rodentium model, which has improved our understanding of pathogenesis and the corresponding host responses. C. Rodentium elicits robust inflammasome-dependent responses in a caspase 1- and caspase 11-dependent manner. Type I interferon signalling is a key factor that regulates inflammasome activation in C. Rodentium infection. The intestinal microbiota is crucial for coordinating mucosal immune responses to C. Rodentium infection, including the development of IgA^+ plasma cells, group 3 innate lymphoid cells (ILC3s; also known as inducible T helper (iT_H) cells), T_H17 cells and T_H22 cells. Defined dietary components, such as vitamin D, vitamin E, selenium, ligands from cruciferous vegetables and polyunsaturated fatty acids (PUFAs), as well as the intestinal microbiota, directly modify mucosal immune responses and epithelial barrier function in response to C. Rodentium infection. Future research using the C. Rodentium model will focus on quantitative proteomics, metabolomics and four-dimensional (4D) imaging studies to unravel pathogen–host–microbiota interactions in unprecedented detail. The mouse pathogen Citrobacter Rodentium has long been used as a model for investigating the pathogenesis of the important enteric human pathogens, enterohaemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC). In this Review, Frankel and colleagues discuss the infection cycle of this pathogen, the mucosal immune response that is elicited and the role of the gut microbiota in preventing colonization. Citrobacter Rodentium is a mucosal pathogen of mice that shares several pathogenic mechanisms with enteropathogenic Escherichia coli (EPEC) and enterohaemorrhagic E. coli (EHEC), which are two clinically important human gastrointestinal pathogens. Thus, C. Rodentium has long been used as a model to understand the molecular basis of EPEC and EHEC infection in vivo . In this Review, we discuss recent studies in which C. Rodentium has been used to study mucosal immunology, including the deregulation of intestinal inflammatory responses during bacteria-induced colitis and the role of the intestinal microbiota in mediating resistance to colonization by enteric pathogens. These insights should help to elucidate the roles of mucosal inflammatory responses and the microbiota in the virulence of enteric pathogens.

Elena M. Comelli - One of the best experts on this subject based on the ideXlab platform.

  • Citrobacter Rodentium alters the mouse colonic miRNome
    Genes & Immunity, 2019
    Co-Authors: Bijun Wen, Amel Taibi, Tomas Tokar, Jianmin Chen, Igor Jurisica, Elena M. Comelli
    Abstract:

    Citrobacter Rodentium is a murine pathogen causing transmissible colonic hyperplasia and colitis with a pathogenic mechanism similar to foodborne enterohaemorrhagic Escherichia coli in humans. Mechanisms underlying intestinal responses to C . Rodentium infection are incompletely understood. We identified 24 colonic microRNAs (miRNAs) as significantly deregulated in response to C . Rodentium , including miR-7a, -17, -19a, -20a, -20b, -92a, -106a, -132, -200a, and -2137; most of these miRNAs belong to the oncogenic miR-17-92 clusters. Pathways involved in cell cycle, cancers, and immune responses were enriched among the predicted targets of these miRNAs. We further demonstrated that an apoptosis facilitator, Bim , is a candidate gene target of miRNA-mediated host response to the infection. These findings suggest that host miRNAs participate in C . Rodentium pathogenesis and may represent novel treatment targets.

  • Effects of Bifidobacterium bifidum in Mice Infected with Citrobacter Rodentium
    Microorganisms, 2019
    Co-Authors: Bijun Wen, Sofia Sagaidak, Amel Taibi, Christopher R Villa, Shin-hann Lee, Elena M. Comelli
    Abstract:

    In vitro and in vivo studies suggest that selected Bifidobacterium bifidum strains sustain intestinal homeostasis. This study aimed to examine whether the administration of B. bifidum MIMBb75 (BB75) attenuates Citrobacter Rodentium infection, a murine model for enteric infection and inflammatory bowel disease in humans. C57Bl6/J mice were randomized to receive BB75 daily starting before or after C. Rodentium infection. BB75 load and infection kinetics were monitored. On day 10 post-infection (p.i.), histological parameters of the large intestine were assessed. Barrier integrity was evaluated by pathogen translocation to secondary organs and in vivo permeability test. Fecal C. Rodentium load peaked at 1010 CFU/g at day 10 p.i., with clearance at day 24 p.i., regardless of probiotic treatment. BB75 administration resulted in 10⁷ cells/g of feces with no effect of timing of administration. BB75 treatment did not attenuate C. Rodentium-induced crypt hyperplasia nor inflammation. C. Rodentium and BB75 can co-exist in the gut with no mutual displacement. However, BB75 cannot counteract C. Rodentium pathology. Our findings provide insight for the understanding of probiotics behavior and their clinical relevance in intestinal inflammation.

  • Development of a real-time PCR assay for quantification of Citrobacter Rodentium.
    Journal of Microbiological Methods, 2016
    Co-Authors: Sofia Sagaidak, Bijun Wen, Amel Taibi, Elena M. Comelli
    Abstract:

    Abstract Molecular tools to quantify Citrobacter Rodentium are not available. We developed a quantitative PCR assay targeting the espB gene. This assay is specific, has a linearity range of about 6.7 × 10 1 to 6.7 × 10 6  cells/PCR reaction (92% efficiency) and a detection limit of about 10 4  cells/g wet feces.

  • Development and Application of a Novel Real-Time PCR Assay for Citrobacter Rodentium Quantification
    The FASEB Journal, 2015
    Co-Authors: Sofia Sagaidak, Bijun Wen, Amel Taibi, Christopher R Villa, Elena M. Comelli
    Abstract:

    Citrobacter Rodentium is a murine pathogen causing transmissible colonic hyperplasia and used to model intestinal colitis including foodborne Escherichia coli O157:H7 pathogenesis. Several probioti...

  • Citrobacter Rodentium Infection Alters Murine Colonic microRNA Signature
    The FASEB Journal, 2015
    Co-Authors: Bijun Wen, Amel Taibi, Jianmin Chen, Elena M. Comelli
    Abstract:

    MicroRNAs (miRs) have been suggested to play a part in the interaction between pathogenic bacteria and host cells. Citrobacter Rodentium is a murine pathogen causing transmissible colonic hyperplasia and colitis with similar pathogenicity as the foodborne enterohaemorrhagic Escherichia coli O157:H7 in humans. This study aimed to examine if colonic microRNA signature is altered during C. Rodentium infection. C57Bl6/J male mice were randomized to C. Rodentium-infected or control group, and sacrificed at the peak of infection (10 days post-infection). Crypt hyperplasia and intestinal inflammation were confirmed by histology and in vivo permeability test. Colonic RNA was used to profile 578 miRs by NanoString technology. Statistics and hierarchical clustering were performed in R. Gene targets of the differentially expressed miRs were identified in silico by prediction algorithms and cross-matching with experimentally verified targets databases. Ninety-four miRs were differentially expressed (p

Ingo Schmitz - One of the best experts on this subject based on the ideXlab platform.