We are analyzing https://link.springer.com/article/10.1186/s40168-017-0278-2.

Title:
Aberrant intestinal microbiota due to IL-1 receptor antagonist deficiency promotes IL-17- and TLR4-dependent arthritis | Microbiome
Description:
Background Perturbation of commensal intestinal microbiota has been associated with several autoimmune diseases. Mice deficient in interleukin-1 receptor antagonist (Il1rn −/− mice) spontaneously develop autoimmune arthritis and are susceptible to other autoimmune diseases such as psoriasis, diabetes, and encephalomyelitis; however, the mechanisms of increased susceptibility to these autoimmune phenotypes are poorly understood. We investigated the role of interleukin-1 receptor antagonist (IL-1Ra) in regulation of commensal intestinal microbiota, and assessed the involvement of microbiota subsets and innate and adaptive mucosal immune responses that underlie the development of spontaneous arthritis in Il1rn −/− mice. Results Using high-throughput 16S rRNA gene sequencing, we show that IL-1Ra critically maintains the diversity and regulates the composition of intestinal microbiota in mice. IL-1Ra deficiency reduced the intestinal microbial diversity and richness, and caused specific taxonomic alterations characterized by overrepresented Helicobacter and underrepresented Ruminococcus and Prevotella. Notably, the aberrant intestinal microbiota in IL1rn −/− mice specifically potentiated IL-17 production by intestinal lamina propria (LP) lymphocytes and skewed the LP T cell balance in favor of T helper 17 (Th17) cells, an effect transferable to WT mice by fecal microbiota. Importantly, LP Th17 cell expansion and the development of spontaneous autoimmune arthritis in IL1rn −/− mice were attenuated under germ-free condition. Selective antibiotic treatment revealed that tobramycin-induced alterations of commensal intestinal microbiota, i.e., reduced Helicobacter, Flexispira, Clostridium, and Dehalobacterium, suppressed arthritis in IL1rn −/− mice. The arthritis phenotype in IL1rn −/− mice was previously shown to depend on Toll-like receptor 4 (TLR4). Using the ablation of both IL-1Ra and TLR4, we here show that the aberrations in the IL1rn −/− microbiota are partly TLR4-dependent. We further identify a role for TLR4 activation in the intestinal lamina propria production of IL-17 and cytokines involved in Th17 differentiation preceding the onset of arthritis. Conclusions These findings identify a critical role for IL1Ra in maintaining the natural diversity and composition of intestinal microbiota, and suggest a role for TLR4 in mucosal Th17 cell induction associated with the development of autoimmune disease in mice.
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Keywords {🔍}

ilrn, mice, arthritis, microbiota, tlr, cells, pubmed, intestinal, article, google, scholar, cas, fig, production, data, role, central, additional, cell, autoimmune, file, figure, microbial, fecal, van, receptor, sfb, commensal, development, analysis, ilra, mucosal, gene, diversity, compared, silp, gut, response, study, specific, sequencing, lamina, propria, tolllike, showed, significant, table, deficiency, interleukin, rrna,

Topics {✒️}

il-1/il-1r antagonist system anti-interleukin-17 monoclonal antibody cd3+cd4+ si-lp cells shahla abdollahi-roodsaz il-1β-induced th17 differentiation th2-related cytokine il-4 segmented filamentous bacteria il-17-producing t-helper cells article download pdf commensal gut-derived bacteria blood monocyte-derived dcs steady-state th17 cells increased th17-inducing activity chronic tlr-mediated arthritis th2-related cytokines il-4 isoamyl alcohol-based extraction real-time quantitative pcr extra-intestinal immune response van den berg joint-adjacent lymph nodes tissue-resident cells participate suppress collagen-induced arthritis il-1ra critically maintains si-lp mononuclear cells tlr-4-mediated interleukin-17 production lineage origin versus human subjects due joint-draining lymph nodes bone marrow-derived cells extra-intestinal il-17 levels si-lp th17 cells autoimmune-prone il1rn−/− mice 16s gene sequencing related subjects tobramycin-sensitive bacteria il-1ra deficiency reduced il-17-producing cells located intestinal lamina propria il-1ra-deficient mice interleukin-1 receptor antagonist cell-dependent gut inflammation lamina propria cells tlr4-mediated modulation microbiota-induced il-1β microbiota-induced il-1beta potentiated th17 response fecal bacterial dna results il-1ra maintains universal bacterial primers gene sequence analysis

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         headline:Aberrant intestinal microbiota due to IL-1 receptor antagonist deficiency promotes IL-17- and TLR4-dependent arthritis
         description:Perturbation of commensal intestinal microbiota has been associated with several autoimmune diseases. Mice deficient in interleukin-1 receptor antagonist (Il1rn −/− mice) spontaneously develop autoimmune arthritis and are susceptible to other autoimmune diseases such as psoriasis, diabetes, and encephalomyelitis; however, the mechanisms of increased susceptibility to these autoimmune phenotypes are poorly understood. We investigated the role of interleukin-1 receptor antagonist (IL-1Ra) in regulation of commensal intestinal microbiota, and assessed the involvement of microbiota subsets and innate and adaptive mucosal immune responses that underlie the development of spontaneous arthritis in Il1rn −/− mice. Using high-throughput 16S rRNA gene sequencing, we show that IL-1Ra critically maintains the diversity and regulates the composition of intestinal microbiota in mice. IL-1Ra deficiency reduced the intestinal microbial diversity and richness, and caused specific taxonomic alterations characterized by overrepresented Helicobacter and underrepresented Ruminococcus and Prevotella. Notably, the aberrant intestinal microbiota in IL1rn −/− mice specifically potentiated IL-17 production by intestinal lamina propria (LP) lymphocytes and skewed the LP T cell balance in favor of T helper 17 (Th17) cells, an effect transferable to WT mice by fecal microbiota. Importantly, LP Th17 cell expansion and the development of spontaneous autoimmune arthritis in IL1rn −/− mice were attenuated under germ-free condition. Selective antibiotic treatment revealed that tobramycin-induced alterations of commensal intestinal microbiota, i.e., reduced Helicobacter, Flexispira, Clostridium, and Dehalobacterium, suppressed arthritis in IL1rn −/− mice. The arthritis phenotype in IL1rn −/− mice was previously shown to depend on Toll-like receptor 4 (TLR4). Using the ablation of both IL-1Ra and TLR4, we here show that the aberrations in the IL1rn −/− microbiota are partly TLR4-dependent. We further identify a role for TLR4 activation in the intestinal lamina propria production of IL-17 and cytokines involved in Th17 differentiation preceding the onset of arthritis. These findings identify a critical role for IL1Ra in maintaining the natural diversity and composition of intestinal microbiota, and suggest a role for TLR4 in mucosal Th17 cell induction associated with the development of autoimmune disease in mice.
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      headline:Aberrant intestinal microbiota due to IL-1 receptor antagonist deficiency promotes IL-17- and TLR4-dependent arthritis
      description:Perturbation of commensal intestinal microbiota has been associated with several autoimmune diseases. Mice deficient in interleukin-1 receptor antagonist (Il1rn −/− mice) spontaneously develop autoimmune arthritis and are susceptible to other autoimmune diseases such as psoriasis, diabetes, and encephalomyelitis; however, the mechanisms of increased susceptibility to these autoimmune phenotypes are poorly understood. We investigated the role of interleukin-1 receptor antagonist (IL-1Ra) in regulation of commensal intestinal microbiota, and assessed the involvement of microbiota subsets and innate and adaptive mucosal immune responses that underlie the development of spontaneous arthritis in Il1rn −/− mice. Using high-throughput 16S rRNA gene sequencing, we show that IL-1Ra critically maintains the diversity and regulates the composition of intestinal microbiota in mice. IL-1Ra deficiency reduced the intestinal microbial diversity and richness, and caused specific taxonomic alterations characterized by overrepresented Helicobacter and underrepresented Ruminococcus and Prevotella. Notably, the aberrant intestinal microbiota in IL1rn −/− mice specifically potentiated IL-17 production by intestinal lamina propria (LP) lymphocytes and skewed the LP T cell balance in favor of T helper 17 (Th17) cells, an effect transferable to WT mice by fecal microbiota. Importantly, LP Th17 cell expansion and the development of spontaneous autoimmune arthritis in IL1rn −/− mice were attenuated under germ-free condition. Selective antibiotic treatment revealed that tobramycin-induced alterations of commensal intestinal microbiota, i.e., reduced Helicobacter, Flexispira, Clostridium, and Dehalobacterium, suppressed arthritis in IL1rn −/− mice. The arthritis phenotype in IL1rn −/− mice was previously shown to depend on Toll-like receptor 4 (TLR4). Using the ablation of both IL-1Ra and TLR4, we here show that the aberrations in the IL1rn −/− microbiota are partly TLR4-dependent. We further identify a role for TLR4 activation in the intestinal lamina propria production of IL-17 and cytokines involved in Th17 differentiation preceding the onset of arthritis. These findings identify a critical role for IL1Ra in maintaining the natural diversity and composition of intestinal microbiota, and suggest a role for TLR4 in mucosal Th17 cell induction associated with the development of autoimmune disease in mice.
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         Autoimmune arthritis
         T helper 17 cells
         Toll-like receptors
         IL-1 receptor antagonist
         Medical Microbiology
         Bioinformatics
         Microbial Ecology
         Microbiology
         Microbial Genetics and Genomics
         Virology
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               type:PostalAddress
            type:Organization
            name:Radboud University Medical Center
            address:
               name:Centre for Molecular and Biomolecular Informatics, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Jos Boekhorst
      affiliation:
            name:Radboud University Medical Center
            address:
               name:Centre for Molecular and Biomolecular Informatics, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
            name:NIZO food research
            address:
               name:NIZO food research, Ede, The Netherlands
               type:PostalAddress
            type:Organization
      name:Harm Wopereis
      affiliation:
            name:Danone Nutricia Research
            address:
               name:Danone Nutricia Research, Utrecht, The Netherlands
               type:PostalAddress
            type:Organization
            name:Wageningen University
            address:
               name:Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Jose U. Scher
      affiliation:
            name:New York University School of Medicine
            address:
               name:Division of Rheumatology, Department of Medicine, New York University School of Medicine, New York, USA
               type:PostalAddress
            type:Organization
      name:Julia Manasson
      affiliation:
            name:New York University School of Medicine
            address:
               name:Division of Rheumatology, Department of Medicine, New York University School of Medicine, New York, USA
               type:PostalAddress
            type:Organization
      name:Sanne J. C. M. Frambach
      affiliation:
            name:Radboud University Medical Center
            address:
               name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Jan Knol
      affiliation:
            name:Danone Nutricia Research
            address:
               name:Danone Nutricia Research, Utrecht, The Netherlands
               type:PostalAddress
            type:Organization
            name:Wageningen University
            address:
               name:Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Johan Garssen
      affiliation:
            name:Danone Nutricia Research
            address:
               name:Danone Nutricia Research, Utrecht, The Netherlands
               type:PostalAddress
            type:Organization
            name:Utrecht University
            address:
               name:Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands
               type:PostalAddress
            type:Organization
      name:Peter M. van der Kraan
      affiliation:
            name:Radboud University Medical Center
            address:
               name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Marije I. Koenders
      affiliation:
            name:Radboud University Medical Center
            address:
               name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Wim B. van den Berg
      affiliation:
            name:Radboud University Medical Center
            address:
               name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Sacha A. F. T. van Hijum
      affiliation:
            name:Radboud University Medical Center
            address:
               name:Centre for Molecular and Biomolecular Informatics, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
            name:NIZO food research
            address:
               name:NIZO food research, Ede, The Netherlands
               type:PostalAddress
            type:Organization
      name:Shahla Abdollahi-Roodsaz
      affiliation:
            name:Radboud University Medical Center
            address:
               name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
               type:PostalAddress
            type:Organization
            name:New York University School of Medicine
            address:
               name:Division of Rheumatology, Department of Medicine, New York University School of Medicine, New York, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
      name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
      name:Centre for Molecular and Biomolecular Informatics, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands
      name:Centre for Molecular and Biomolecular Informatics, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands
      name:NIZO food research, Ede, The Netherlands
      name:Danone Nutricia Research, Utrecht, The Netherlands
      name:Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands
      name:Division of Rheumatology, Department of Medicine, New York University School of Medicine, New York, USA
      name:Division of Rheumatology, Department of Medicine, New York University School of Medicine, New York, USA
      name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
      name:Danone Nutricia Research, Utrecht, The Netherlands
      name:Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands
      name:Danone Nutricia Research, Utrecht, The Netherlands
      name:Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands
      name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
      name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
      name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
      name:Centre for Molecular and Biomolecular Informatics, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands
      name:NIZO food research, Ede, The Netherlands
      name:Experimental Rheumatology (272), Radboud University Medical Center, Nijmegen, The Netherlands
      name:Division of Rheumatology, Department of Medicine, New York University School of Medicine, New York, USA

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