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Adrien Six - One of the best experts on this subject based on the ideXlab platform.

  • the regenerating family member 3 β instigates il 17a mediated neutrophil recruitment downstream of nod1 2 signalling for controlling Colonisation Resistance independently of microbiota community structure
    Gut, 2019
    Co-Authors: Nadine Waldschmitt, Bruno Lamas, Hang-phuong Pham, Vassiliki Zacharioudaki, Myriam Delacre, Sho Kitamoto, Thomas Secher, Olivier Boulard, Emilie Floquet, Adrien Six
    Abstract:

    Objective Loss of the Crohn’s disease predisposing NOD2 gene results in an intestinal microenvironment conducive for Colonisation by attaching-and-effacing enteropathogens. However, it remains elusive whether it relies on the intracellular recruitment of the serine-threonine kinase RIPK2 by NOD2, a step that is required for its activation of the transcription factor NF-κB. Design Colonisation Resistance was evaluated in wild type and mutant mice, as well as in ex-germ-free (ex-GF) mice which were colonised either with faeces from Ripk2-deficient mice or with bacteria with similar preferences for carbohydrates to those acquired by the pathogen. The severity of the mucosal pathology was quantified at several time points postinfection by using a previously established scoring. The community resilience in response to infection was evaluated by 16S ribosomal RNA gene sequence analysis. The control of pathogen virulence was evaluated by monitoring the secretion of Citrobacter-specific antibody response in the faeces. Results Primary infection was similarly outcompeted in ex-GF Ripk2-deficient and control mice, demonstrating that the susceptibility to infection resulting from RIPK2 deficiency cannot be solely attributed to specific microbiota community structures. In contrast, delayed clearance of Citrobacter rodentium and exacerbated histopathology were preceded by a weakened propensity of intestinal macrophages to afford innate lymphoid cell activation. This tissue protection unexpectedly required the regenerating family member 3β by instigating interleukin (IL) 17A-mediated neutrophil recruitment to the intestine and subsequent phosphorylation of signal transducer and activator of transcription 3. Conclusions These results unveil a previously unrecognised mechanism that efficiently protects from Colonisation by diarrhoeagenic bacteria early in infection.

Nadine Waldschmitt - One of the best experts on this subject based on the ideXlab platform.

  • the regenerating family member 3 β instigates il 17a mediated neutrophil recruitment downstream of nod1 2 signalling for controlling Colonisation Resistance independently of microbiota community structure
    Gut, 2019
    Co-Authors: Nadine Waldschmitt, Bruno Lamas, Hang-phuong Pham, Vassiliki Zacharioudaki, Myriam Delacre, Sho Kitamoto, Thomas Secher, Olivier Boulard, Emilie Floquet, Adrien Six
    Abstract:

    Objective Loss of the Crohn’s disease predisposing NOD2 gene results in an intestinal microenvironment conducive for Colonisation by attaching-and-effacing enteropathogens. However, it remains elusive whether it relies on the intracellular recruitment of the serine-threonine kinase RIPK2 by NOD2, a step that is required for its activation of the transcription factor NF-κB. Design Colonisation Resistance was evaluated in wild type and mutant mice, as well as in ex-germ-free (ex-GF) mice which were colonised either with faeces from Ripk2-deficient mice or with bacteria with similar preferences for carbohydrates to those acquired by the pathogen. The severity of the mucosal pathology was quantified at several time points postinfection by using a previously established scoring. The community resilience in response to infection was evaluated by 16S ribosomal RNA gene sequence analysis. The control of pathogen virulence was evaluated by monitoring the secretion of Citrobacter-specific antibody response in the faeces. Results Primary infection was similarly outcompeted in ex-GF Ripk2-deficient and control mice, demonstrating that the susceptibility to infection resulting from RIPK2 deficiency cannot be solely attributed to specific microbiota community structures. In contrast, delayed clearance of Citrobacter rodentium and exacerbated histopathology were preceded by a weakened propensity of intestinal macrophages to afford innate lymphoid cell activation. This tissue protection unexpectedly required the regenerating family member 3β by instigating interleukin (IL) 17A-mediated neutrophil recruitment to the intestine and subsequent phosphorylation of signal transducer and activator of transcription 3. Conclusions These results unveil a previously unrecognised mechanism that efficiently protects from Colonisation by diarrhoeagenic bacteria early in infection.

  • Card9 mediates susceptibility to intestinal pathogens through microbiota modulation and control of bacterial virulence
    Gut, 2017
    Co-Authors: Bruno Lamas, Marie-laure Michel, Nadine Waldschmitt, Hang-phuong Pham, Vassiliki Zacharioudaki, Louise Dupraz, Myriam Delacre, Jane M Natividad, Gregory Da Costa, Julien Planchais
    Abstract:

    Objective: In association with innate and adaptive immunity, the microbiota controls the Colonisation Resistance against intestinal pathogens. Caspase recruitment domain 9 (CARD9), a key innate immunity gene, is required to shape a normal gut microbiota. Card9–/– mice are more susceptible to the enteric mouse pathogen Citrobacter rodentium that mimics human infections with enteropathogenic and enterohaemorrhagic Escherichia coli. Here, we examined how CARD9 controls C. rodentium infection susceptibility through microbiota-dependent and microbiota-independent mechanisms. Design: C. rodentium infection was assessed in conventional and germ-free (GF) wild-type (WT) and Card9–/– mice. To explore the impact of Card9–/–microbiota in infection susceptibility, GF WT mice were colonised with WT (WT→GF) or Card9–/– (Card9–/–→GF) microbiota before C. rodentium infection. Microbiota composition was determined by 16S rDNA gene sequencing. Inflammation severity was determined by histology score and lipocalin level. Microbiota–host immune system interactions were assessed by quantitative PCR analysis. Results: CARD9 controls pathogen virulence in a microbiota-independent manner by supporting a specific humoral response. Higher susceptibility to C. rodentium-induced colitis was observed in Card9–/–→GF mice. The microbiota of Card9–/– mice failed to outcompete the monosaccharide-consuming C. rodentium, worsening the infection severity. A polysaccharide-enriched diet counteracted the ecological advantage of C. rodentium and the defective pathogen-specific antibody response in Card9–/– mice. Conclusions: CARD9 modulates the susceptibility to intestinal infection by controlling the pathogen virulence in a microbiota-dependent and microbiota-independent manner. Genetic susceptibility to intestinal pathogens can be overridden by diet intervention that restores humoural immunity and a competing microbiota.

Bruno Lamas - One of the best experts on this subject based on the ideXlab platform.

  • the regenerating family member 3 β instigates il 17a mediated neutrophil recruitment downstream of nod1 2 signalling for controlling Colonisation Resistance independently of microbiota community structure
    Gut, 2019
    Co-Authors: Nadine Waldschmitt, Bruno Lamas, Hang-phuong Pham, Vassiliki Zacharioudaki, Myriam Delacre, Sho Kitamoto, Thomas Secher, Olivier Boulard, Emilie Floquet, Adrien Six
    Abstract:

    Objective Loss of the Crohn’s disease predisposing NOD2 gene results in an intestinal microenvironment conducive for Colonisation by attaching-and-effacing enteropathogens. However, it remains elusive whether it relies on the intracellular recruitment of the serine-threonine kinase RIPK2 by NOD2, a step that is required for its activation of the transcription factor NF-κB. Design Colonisation Resistance was evaluated in wild type and mutant mice, as well as in ex-germ-free (ex-GF) mice which were colonised either with faeces from Ripk2-deficient mice or with bacteria with similar preferences for carbohydrates to those acquired by the pathogen. The severity of the mucosal pathology was quantified at several time points postinfection by using a previously established scoring. The community resilience in response to infection was evaluated by 16S ribosomal RNA gene sequence analysis. The control of pathogen virulence was evaluated by monitoring the secretion of Citrobacter-specific antibody response in the faeces. Results Primary infection was similarly outcompeted in ex-GF Ripk2-deficient and control mice, demonstrating that the susceptibility to infection resulting from RIPK2 deficiency cannot be solely attributed to specific microbiota community structures. In contrast, delayed clearance of Citrobacter rodentium and exacerbated histopathology were preceded by a weakened propensity of intestinal macrophages to afford innate lymphoid cell activation. This tissue protection unexpectedly required the regenerating family member 3β by instigating interleukin (IL) 17A-mediated neutrophil recruitment to the intestine and subsequent phosphorylation of signal transducer and activator of transcription 3. Conclusions These results unveil a previously unrecognised mechanism that efficiently protects from Colonisation by diarrhoeagenic bacteria early in infection.

  • Card9 mediates susceptibility to intestinal pathogens through microbiota modulation and control of bacterial virulence
    Gut, 2017
    Co-Authors: Bruno Lamas, Marie-laure Michel, Nadine Waldschmitt, Hang-phuong Pham, Vassiliki Zacharioudaki, Louise Dupraz, Myriam Delacre, Jane M Natividad, Gregory Da Costa, Julien Planchais
    Abstract:

    Objective: In association with innate and adaptive immunity, the microbiota controls the Colonisation Resistance against intestinal pathogens. Caspase recruitment domain 9 (CARD9), a key innate immunity gene, is required to shape a normal gut microbiota. Card9–/– mice are more susceptible to the enteric mouse pathogen Citrobacter rodentium that mimics human infections with enteropathogenic and enterohaemorrhagic Escherichia coli. Here, we examined how CARD9 controls C. rodentium infection susceptibility through microbiota-dependent and microbiota-independent mechanisms. Design: C. rodentium infection was assessed in conventional and germ-free (GF) wild-type (WT) and Card9–/– mice. To explore the impact of Card9–/–microbiota in infection susceptibility, GF WT mice were colonised with WT (WT→GF) or Card9–/– (Card9–/–→GF) microbiota before C. rodentium infection. Microbiota composition was determined by 16S rDNA gene sequencing. Inflammation severity was determined by histology score and lipocalin level. Microbiota–host immune system interactions were assessed by quantitative PCR analysis. Results: CARD9 controls pathogen virulence in a microbiota-independent manner by supporting a specific humoral response. Higher susceptibility to C. rodentium-induced colitis was observed in Card9–/–→GF mice. The microbiota of Card9–/– mice failed to outcompete the monosaccharide-consuming C. rodentium, worsening the infection severity. A polysaccharide-enriched diet counteracted the ecological advantage of C. rodentium and the defective pathogen-specific antibody response in Card9–/– mice. Conclusions: CARD9 modulates the susceptibility to intestinal infection by controlling the pathogen virulence in a microbiota-dependent and microbiota-independent manner. Genetic susceptibility to intestinal pathogens can be overridden by diet intervention that restores humoural immunity and a competing microbiota.

Hang-phuong Pham - One of the best experts on this subject based on the ideXlab platform.

  • the regenerating family member 3 β instigates il 17a mediated neutrophil recruitment downstream of nod1 2 signalling for controlling Colonisation Resistance independently of microbiota community structure
    Gut, 2019
    Co-Authors: Nadine Waldschmitt, Bruno Lamas, Hang-phuong Pham, Vassiliki Zacharioudaki, Myriam Delacre, Sho Kitamoto, Thomas Secher, Olivier Boulard, Emilie Floquet, Adrien Six
    Abstract:

    Objective Loss of the Crohn’s disease predisposing NOD2 gene results in an intestinal microenvironment conducive for Colonisation by attaching-and-effacing enteropathogens. However, it remains elusive whether it relies on the intracellular recruitment of the serine-threonine kinase RIPK2 by NOD2, a step that is required for its activation of the transcription factor NF-κB. Design Colonisation Resistance was evaluated in wild type and mutant mice, as well as in ex-germ-free (ex-GF) mice which were colonised either with faeces from Ripk2-deficient mice or with bacteria with similar preferences for carbohydrates to those acquired by the pathogen. The severity of the mucosal pathology was quantified at several time points postinfection by using a previously established scoring. The community resilience in response to infection was evaluated by 16S ribosomal RNA gene sequence analysis. The control of pathogen virulence was evaluated by monitoring the secretion of Citrobacter-specific antibody response in the faeces. Results Primary infection was similarly outcompeted in ex-GF Ripk2-deficient and control mice, demonstrating that the susceptibility to infection resulting from RIPK2 deficiency cannot be solely attributed to specific microbiota community structures. In contrast, delayed clearance of Citrobacter rodentium and exacerbated histopathology were preceded by a weakened propensity of intestinal macrophages to afford innate lymphoid cell activation. This tissue protection unexpectedly required the regenerating family member 3β by instigating interleukin (IL) 17A-mediated neutrophil recruitment to the intestine and subsequent phosphorylation of signal transducer and activator of transcription 3. Conclusions These results unveil a previously unrecognised mechanism that efficiently protects from Colonisation by diarrhoeagenic bacteria early in infection.

  • Card9 mediates susceptibility to intestinal pathogens through microbiota modulation and control of bacterial virulence
    Gut, 2017
    Co-Authors: Bruno Lamas, Marie-laure Michel, Nadine Waldschmitt, Hang-phuong Pham, Vassiliki Zacharioudaki, Louise Dupraz, Myriam Delacre, Jane M Natividad, Gregory Da Costa, Julien Planchais
    Abstract:

    Objective: In association with innate and adaptive immunity, the microbiota controls the Colonisation Resistance against intestinal pathogens. Caspase recruitment domain 9 (CARD9), a key innate immunity gene, is required to shape a normal gut microbiota. Card9–/– mice are more susceptible to the enteric mouse pathogen Citrobacter rodentium that mimics human infections with enteropathogenic and enterohaemorrhagic Escherichia coli. Here, we examined how CARD9 controls C. rodentium infection susceptibility through microbiota-dependent and microbiota-independent mechanisms. Design: C. rodentium infection was assessed in conventional and germ-free (GF) wild-type (WT) and Card9–/– mice. To explore the impact of Card9–/–microbiota in infection susceptibility, GF WT mice were colonised with WT (WT→GF) or Card9–/– (Card9–/–→GF) microbiota before C. rodentium infection. Microbiota composition was determined by 16S rDNA gene sequencing. Inflammation severity was determined by histology score and lipocalin level. Microbiota–host immune system interactions were assessed by quantitative PCR analysis. Results: CARD9 controls pathogen virulence in a microbiota-independent manner by supporting a specific humoral response. Higher susceptibility to C. rodentium-induced colitis was observed in Card9–/–→GF mice. The microbiota of Card9–/– mice failed to outcompete the monosaccharide-consuming C. rodentium, worsening the infection severity. A polysaccharide-enriched diet counteracted the ecological advantage of C. rodentium and the defective pathogen-specific antibody response in Card9–/– mice. Conclusions: CARD9 modulates the susceptibility to intestinal infection by controlling the pathogen virulence in a microbiota-dependent and microbiota-independent manner. Genetic susceptibility to intestinal pathogens can be overridden by diet intervention that restores humoural immunity and a competing microbiota.

Myriam Delacre - One of the best experts on this subject based on the ideXlab platform.

  • the regenerating family member 3 β instigates il 17a mediated neutrophil recruitment downstream of nod1 2 signalling for controlling Colonisation Resistance independently of microbiota community structure
    Gut, 2019
    Co-Authors: Nadine Waldschmitt, Bruno Lamas, Hang-phuong Pham, Vassiliki Zacharioudaki, Myriam Delacre, Sho Kitamoto, Thomas Secher, Olivier Boulard, Emilie Floquet, Adrien Six
    Abstract:

    Objective Loss of the Crohn’s disease predisposing NOD2 gene results in an intestinal microenvironment conducive for Colonisation by attaching-and-effacing enteropathogens. However, it remains elusive whether it relies on the intracellular recruitment of the serine-threonine kinase RIPK2 by NOD2, a step that is required for its activation of the transcription factor NF-κB. Design Colonisation Resistance was evaluated in wild type and mutant mice, as well as in ex-germ-free (ex-GF) mice which were colonised either with faeces from Ripk2-deficient mice or with bacteria with similar preferences for carbohydrates to those acquired by the pathogen. The severity of the mucosal pathology was quantified at several time points postinfection by using a previously established scoring. The community resilience in response to infection was evaluated by 16S ribosomal RNA gene sequence analysis. The control of pathogen virulence was evaluated by monitoring the secretion of Citrobacter-specific antibody response in the faeces. Results Primary infection was similarly outcompeted in ex-GF Ripk2-deficient and control mice, demonstrating that the susceptibility to infection resulting from RIPK2 deficiency cannot be solely attributed to specific microbiota community structures. In contrast, delayed clearance of Citrobacter rodentium and exacerbated histopathology were preceded by a weakened propensity of intestinal macrophages to afford innate lymphoid cell activation. This tissue protection unexpectedly required the regenerating family member 3β by instigating interleukin (IL) 17A-mediated neutrophil recruitment to the intestine and subsequent phosphorylation of signal transducer and activator of transcription 3. Conclusions These results unveil a previously unrecognised mechanism that efficiently protects from Colonisation by diarrhoeagenic bacteria early in infection.

  • Card9 mediates susceptibility to intestinal pathogens through microbiota modulation and control of bacterial virulence
    Gut, 2017
    Co-Authors: Bruno Lamas, Marie-laure Michel, Nadine Waldschmitt, Hang-phuong Pham, Vassiliki Zacharioudaki, Louise Dupraz, Myriam Delacre, Jane M Natividad, Gregory Da Costa, Julien Planchais
    Abstract:

    Objective: In association with innate and adaptive immunity, the microbiota controls the Colonisation Resistance against intestinal pathogens. Caspase recruitment domain 9 (CARD9), a key innate immunity gene, is required to shape a normal gut microbiota. Card9–/– mice are more susceptible to the enteric mouse pathogen Citrobacter rodentium that mimics human infections with enteropathogenic and enterohaemorrhagic Escherichia coli. Here, we examined how CARD9 controls C. rodentium infection susceptibility through microbiota-dependent and microbiota-independent mechanisms. Design: C. rodentium infection was assessed in conventional and germ-free (GF) wild-type (WT) and Card9–/– mice. To explore the impact of Card9–/–microbiota in infection susceptibility, GF WT mice were colonised with WT (WT→GF) or Card9–/– (Card9–/–→GF) microbiota before C. rodentium infection. Microbiota composition was determined by 16S rDNA gene sequencing. Inflammation severity was determined by histology score and lipocalin level. Microbiota–host immune system interactions were assessed by quantitative PCR analysis. Results: CARD9 controls pathogen virulence in a microbiota-independent manner by supporting a specific humoral response. Higher susceptibility to C. rodentium-induced colitis was observed in Card9–/–→GF mice. The microbiota of Card9–/– mice failed to outcompete the monosaccharide-consuming C. rodentium, worsening the infection severity. A polysaccharide-enriched diet counteracted the ecological advantage of C. rodentium and the defective pathogen-specific antibody response in Card9–/– mice. Conclusions: CARD9 modulates the susceptibility to intestinal infection by controlling the pathogen virulence in a microbiota-dependent and microbiota-independent manner. Genetic susceptibility to intestinal pathogens can be overridden by diet intervention that restores humoural immunity and a competing microbiota.