Dietary tryptophan links encephalogenicity of autoreactive T cells with gut microbial ecology

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Dietary tryptophan links encephalogenicity of autoreactive T cells with gut microbial ecology. / Sonner, Jana K; Keil, Melanie; Falk-Paulsen, Maren; Mishra, Neha; Rehman, Ateequr; Kramer, Magdalena; Deumelandt, Katrin; Röwe, Julian; Sanghvi, Khwab; Wolf, Lara; von Landenberg, Anna; Wolff, Hendrik; Bharti, Richa; Oezen, Iris; Lanz, Tobias V; Wanke, Florian; Tang, Yilang; Brandao, Ines; Mohapatra, Soumya R; Epping, Lisa; Grill, Alexandra; Röth, Ralph; Niesler, Beate; Meuth, Sven G; Opitz, Christiane A; Okun, Jürgen G; Reinhardt, Christoph; Kurschus, Florian C; Wick, Wolfgang; Bode, Helge B; Rosenstiel, Philip; Platten, Michael.

in: NAT COMMUN, Jahrgang 10, Nr. 1, 25.10.2019, S. 4877.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Sonner, JK, Keil, M, Falk-Paulsen, M, Mishra, N, Rehman, A, Kramer, M, Deumelandt, K, Röwe, J, Sanghvi, K, Wolf, L, von Landenberg, A, Wolff, H, Bharti, R, Oezen, I, Lanz, TV, Wanke, F, Tang, Y, Brandao, I, Mohapatra, SR, Epping, L, Grill, A, Röth, R, Niesler, B, Meuth, SG, Opitz, CA, Okun, JG, Reinhardt, C, Kurschus, FC, Wick, W, Bode, HB, Rosenstiel, P & Platten, M 2019, 'Dietary tryptophan links encephalogenicity of autoreactive T cells with gut microbial ecology', NAT COMMUN, Jg. 10, Nr. 1, S. 4877. https://doi.org/10.1038/s41467-019-12776-4

APA

Sonner, J. K., Keil, M., Falk-Paulsen, M., Mishra, N., Rehman, A., Kramer, M., Deumelandt, K., Röwe, J., Sanghvi, K., Wolf, L., von Landenberg, A., Wolff, H., Bharti, R., Oezen, I., Lanz, T. V., Wanke, F., Tang, Y., Brandao, I., Mohapatra, S. R., ... Platten, M. (2019). Dietary tryptophan links encephalogenicity of autoreactive T cells with gut microbial ecology. NAT COMMUN, 10(1), 4877. https://doi.org/10.1038/s41467-019-12776-4

Vancouver

Bibtex

@article{6e980f6144354d5c8123e609197ac3f5,
title = "Dietary tryptophan links encephalogenicity of autoreactive T cells with gut microbial ecology",
abstract = "The interaction between the mammalian host and its resident gut microbiota is known to license adaptive immune responses. Nutritional constituents strongly influence composition and functional properties of the intestinal microbial communities. Here, we report that omission of a single essential amino acid - tryptophan - from the diet abrogates CNS autoimmunity in a mouse model of multiple sclerosis. Dietary tryptophan restriction results in impaired encephalitogenic T cell responses and is accompanied by a mild intestinal inflammatory response and a profound phenotypic shift of gut microbiota. Protective effects of dietary tryptophan restriction are abrogated in germ-free mice, but are independent of canonical host sensors of intracellular tryptophan metabolites. We conclude that dietary tryptophan restriction alters metabolic properties of gut microbiota, which in turn have an impact on encephalitogenic T cell responses. This link between gut microbiota, dietary tryptophan and adaptive immunity may help to develop therapeutic strategies for protection from autoimmune neuroinflammation.",
keywords = "Animals, Autoimmunity/immunology, Diet, Dietary Proteins, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental/immunology, Gastrointestinal Microbiome/genetics, Mice, Multiple Sclerosis, RNA, Ribosomal, 16S/genetics, T-Lymphocytes/immunology, Tryptophan",
author = "Sonner, {Jana K} and Melanie Keil and Maren Falk-Paulsen and Neha Mishra and Ateequr Rehman and Magdalena Kramer and Katrin Deumelandt and Julian R{\"o}we and Khwab Sanghvi and Lara Wolf and {von Landenberg}, Anna and Hendrik Wolff and Richa Bharti and Iris Oezen and Lanz, {Tobias V} and Florian Wanke and Yilang Tang and Ines Brandao and Mohapatra, {Soumya R} and Lisa Epping and Alexandra Grill and Ralph R{\"o}th and Beate Niesler and Meuth, {Sven G} and Opitz, {Christiane A} and Okun, {J{\"u}rgen G} and Christoph Reinhardt and Kurschus, {Florian C} and Wolfgang Wick and Bode, {Helge B} and Philip Rosenstiel and Michael Platten",
year = "2019",
month = oct,
day = "25",
doi = "10.1038/s41467-019-12776-4",
language = "English",
volume = "10",
pages = "4877",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Dietary tryptophan links encephalogenicity of autoreactive T cells with gut microbial ecology

AU - Sonner, Jana K

AU - Keil, Melanie

AU - Falk-Paulsen, Maren

AU - Mishra, Neha

AU - Rehman, Ateequr

AU - Kramer, Magdalena

AU - Deumelandt, Katrin

AU - Röwe, Julian

AU - Sanghvi, Khwab

AU - Wolf, Lara

AU - von Landenberg, Anna

AU - Wolff, Hendrik

AU - Bharti, Richa

AU - Oezen, Iris

AU - Lanz, Tobias V

AU - Wanke, Florian

AU - Tang, Yilang

AU - Brandao, Ines

AU - Mohapatra, Soumya R

AU - Epping, Lisa

AU - Grill, Alexandra

AU - Röth, Ralph

AU - Niesler, Beate

AU - Meuth, Sven G

AU - Opitz, Christiane A

AU - Okun, Jürgen G

AU - Reinhardt, Christoph

AU - Kurschus, Florian C

AU - Wick, Wolfgang

AU - Bode, Helge B

AU - Rosenstiel, Philip

AU - Platten, Michael

PY - 2019/10/25

Y1 - 2019/10/25

N2 - The interaction between the mammalian host and its resident gut microbiota is known to license adaptive immune responses. Nutritional constituents strongly influence composition and functional properties of the intestinal microbial communities. Here, we report that omission of a single essential amino acid - tryptophan - from the diet abrogates CNS autoimmunity in a mouse model of multiple sclerosis. Dietary tryptophan restriction results in impaired encephalitogenic T cell responses and is accompanied by a mild intestinal inflammatory response and a profound phenotypic shift of gut microbiota. Protective effects of dietary tryptophan restriction are abrogated in germ-free mice, but are independent of canonical host sensors of intracellular tryptophan metabolites. We conclude that dietary tryptophan restriction alters metabolic properties of gut microbiota, which in turn have an impact on encephalitogenic T cell responses. This link between gut microbiota, dietary tryptophan and adaptive immunity may help to develop therapeutic strategies for protection from autoimmune neuroinflammation.

AB - The interaction between the mammalian host and its resident gut microbiota is known to license adaptive immune responses. Nutritional constituents strongly influence composition and functional properties of the intestinal microbial communities. Here, we report that omission of a single essential amino acid - tryptophan - from the diet abrogates CNS autoimmunity in a mouse model of multiple sclerosis. Dietary tryptophan restriction results in impaired encephalitogenic T cell responses and is accompanied by a mild intestinal inflammatory response and a profound phenotypic shift of gut microbiota. Protective effects of dietary tryptophan restriction are abrogated in germ-free mice, but are independent of canonical host sensors of intracellular tryptophan metabolites. We conclude that dietary tryptophan restriction alters metabolic properties of gut microbiota, which in turn have an impact on encephalitogenic T cell responses. This link between gut microbiota, dietary tryptophan and adaptive immunity may help to develop therapeutic strategies for protection from autoimmune neuroinflammation.

KW - Animals

KW - Autoimmunity/immunology

KW - Diet

KW - Dietary Proteins

KW - Disease Models, Animal

KW - Encephalomyelitis, Autoimmune, Experimental/immunology

KW - Gastrointestinal Microbiome/genetics

KW - Mice

KW - Multiple Sclerosis

KW - RNA, Ribosomal, 16S/genetics

KW - T-Lymphocytes/immunology

KW - Tryptophan

U2 - 10.1038/s41467-019-12776-4

DO - 10.1038/s41467-019-12776-4

M3 - SCORING: Journal article

C2 - 31653831

VL - 10

SP - 4877

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

ER -