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Salt-responsive gut commensal modulates TH17 axis and disease.
Wilck, Nicola; Matus, Mariana G; Kearney, Sean M; Olesen, Scott W; Forslund, Kristoffer; Bartolomaeus, Hendrik; Haase, Stefanie; Mähler, Anja; Balogh, András; Markó, Lajos; Vvedenskaya, Olga; Kleiner, Friedrich H; Tsvetkov, Dmitry; Klug, Lars; Costea, Paul I; Sunagawa, Shinichi; Maier, Lisa; Rakova, Natalia; Schatz, Valentin; Neubert, Patrick; Frätzer, Christian; Krannich, Alexander; Gollasch, Maik; Grohme, Diana A; Côrte-Real, Beatriz F; Gerlach, Roman G; Basic, Marijana; Typas, Athanasios; Wu, Chuan; Titze, Jens M; Jantsch, Jonathan; Boschmann, Michael; Dechend, Ralf; Kleinewietfeld, Markus; Kempa, Stefan; Bork, Peer; Linker, Ralf A; Alm, Eric J; Müller, Dominik N.
Afiliação
  • Wilck N; Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
  • Matus MG; Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
  • Kearney SM; Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
  • Olesen SW; DZHK (German Centre for Cardiovascular Research), partner site Berlin, Germany.
  • Forslund K; Berlin Institute of Health (BIH), Berlin, Germany.
  • Bartolomaeus H; Center for Microbiome Informatics and Therapeutics, and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
  • Haase S; Computational and Systems Biology Program, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
  • Mähler A; Center for Microbiome Informatics and Therapeutics, and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
  • Balogh A; Center for Microbiome Informatics and Therapeutics, and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
  • Markó L; European Molecular Biology Laboratory, Structural and Computational Biology Unit, 69117 Heidelberg, Germany.
  • Vvedenskaya O; Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
  • Kleiner FH; Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
  • Tsvetkov D; Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
  • Klug L; DZHK (German Centre for Cardiovascular Research), partner site Berlin, Germany.
  • Costea PI; Department of Neurology, Friedrich-Alexander-University Erlangen-Nuremberg, 91054 Erlangen, Germany.
  • Sunagawa S; Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
  • Maier L; Berlin Institute of Health (BIH), Berlin, Germany.
  • Rakova N; Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
  • Schatz V; Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
  • Neubert P; Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
  • Frätzer C; DZHK (German Centre for Cardiovascular Research), partner site Berlin, Germany.
  • Krannich A; Berlin Institute of Health (BIH), Berlin, Germany.
  • Gollasch M; Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
  • Grohme DA; Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
  • Côrte-Real BF; Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
  • Gerlach RG; DZHK (German Centre for Cardiovascular Research), partner site Berlin, Germany.
  • Basic M; Berlin Institute of Health (BIH), Berlin, Germany.
  • Typas A; Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
  • Wu C; Integrative Proteomics and Metabolomics Platform, Berlin Institute for Medical Systems Biology BIMSB, 13125 Berlin, Germany.
  • Titze JM; Berlin School of Integrative Oncology, Charité University Medicine Berlin, Berlin, Germany.
  • Jantsch J; Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
  • Boschmann M; Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
  • Dechend R; Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
  • Kleinewietfeld M; Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
  • Kempa S; Berlin Institute of Health (BIH), Berlin, Germany.
  • Bork P; European Molecular Biology Laboratory, Structural and Computational Biology Unit, 69117 Heidelberg, Germany.
  • Linker RA; European Molecular Biology Laboratory, Structural and Computational Biology Unit, 69117 Heidelberg, Germany.
  • Alm EJ; Institute of Microbiology, ETH Zurich, 8092 Zurich, Switzerland.
  • Müller DN; European Molecular Biology Laboratory, Genome Biology Unit, 69117 Heidelberg, Germany.
Nature ; 551(7682): 585-589, 2017 11 30.
Article em En | MEDLINE | ID: mdl-29143823
A Western lifestyle with high salt consumption can lead to hypertension and cardiovascular disease. High salt may additionally drive autoimmunity by inducing T helper 17 (TH17) cells, which can also contribute to hypertension. Induction of TH17 cells depends on gut microbiota; however, the effect of salt on the gut microbiome is unknown. Here we show that high salt intake affects the gut microbiome in mice, particularly by depleting Lactobacillus murinus. Consequently, treatment of mice with L. murinus prevented salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating TH17 cells. In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced intestinal survival of Lactobacillus spp., increased TH17 cells and increased blood pressure. Our results connect high salt intake to the gut-immune axis and highlight the gut microbiome as a potential therapeutic target to counteract salt-sensitive conditions.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Cloreto de Sódio / Células Th17 / Microbioma Gastrointestinal / Lactobacillus Tipo de estudo: Prognostic_studies Limite: Animals / Humans / Male Idioma: En Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Cloreto de Sódio / Células Th17 / Microbioma Gastrointestinal / Lactobacillus Tipo de estudo: Prognostic_studies Limite: Animals / Humans / Male Idioma: En Ano de publicação: 2017 Tipo de documento: Article