A microbially produced AhR ligand promotes a Tph1-driven tolerogenic program in multiple sclerosis
Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of...
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2024 |
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In: Scientific Reports - Nature Portfolio, 2011, 14(2024), 1, Seite 16 |
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volume:14 ; year:2024 ; number:1 ; pages:16 |
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DOI / URN: |
10.1038/s41598-024-57400-8 |
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DOAJ095739025 |
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520 | |a Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. | ||
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10.1038/s41598-024-57400-8 doi (DE-627)DOAJ095739025 (DE-599)DOAJef3dd28764624aada7153b8839b12acc DE-627 ger DE-627 rakwb eng Teresa Zelante verfasserin aut A microbially produced AhR ligand promotes a Tph1-driven tolerogenic program in multiple sclerosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. Mast cells Aryl hydrocarbon receptor Serotonin 3-IAld Multiple sclerosis Medicine R Science Q Giuseppe Paolicelli verfasserin aut Francesca Fallarino verfasserin aut Marco Gargaro verfasserin aut Gianluca Vascelli verfasserin aut Marco De Zuani verfasserin aut Jan Fric verfasserin aut Petra Laznickova verfasserin aut Marcela Hortova Kohoutkova verfasserin aut Antonio Macchiarulo verfasserin aut Daniela Dolciami verfasserin aut Giuseppe Pieraccini verfasserin aut Lorenzo Gaetani verfasserin aut Giulia Scalisi verfasserin aut Caterina Trevisan verfasserin aut Barbara Frossi verfasserin aut Carlo Pucillo verfasserin aut Antonella De Luca verfasserin aut Emilia Nunzi verfasserin aut Roberta Spaccapelo verfasserin aut Marilena Pariano verfasserin aut Monica Borghi verfasserin aut Francesca Boscaro verfasserin aut Riccardo Romoli verfasserin aut Andrea Mancini verfasserin aut Lucia Gentili verfasserin aut Giorgia Renga verfasserin aut Claudio Costantini verfasserin aut Matteo Puccetti verfasserin aut Stefano Giovagnoli verfasserin aut Maurizio Ricci verfasserin aut Martina Antonini verfasserin aut Paolo Calabresi verfasserin aut Paolo Puccetti verfasserin aut Massimiliano Di Filippo verfasserin aut Luigina Romani verfasserin aut In Scientific Reports Nature Portfolio, 2011 14(2024), 1, Seite 16 (DE-627)663366712 (DE-600)2615211-3 20452322 nnns volume:14 year:2024 number:1 pages:16 https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/article/ef3dd28764624aada7153b8839b12acc kostenfrei https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/toc/2045-2322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2024 1 16 |
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10.1038/s41598-024-57400-8 doi (DE-627)DOAJ095739025 (DE-599)DOAJef3dd28764624aada7153b8839b12acc DE-627 ger DE-627 rakwb eng Teresa Zelante verfasserin aut A microbially produced AhR ligand promotes a Tph1-driven tolerogenic program in multiple sclerosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. Mast cells Aryl hydrocarbon receptor Serotonin 3-IAld Multiple sclerosis Medicine R Science Q Giuseppe Paolicelli verfasserin aut Francesca Fallarino verfasserin aut Marco Gargaro verfasserin aut Gianluca Vascelli verfasserin aut Marco De Zuani verfasserin aut Jan Fric verfasserin aut Petra Laznickova verfasserin aut Marcela Hortova Kohoutkova verfasserin aut Antonio Macchiarulo verfasserin aut Daniela Dolciami verfasserin aut Giuseppe Pieraccini verfasserin aut Lorenzo Gaetani verfasserin aut Giulia Scalisi verfasserin aut Caterina Trevisan verfasserin aut Barbara Frossi verfasserin aut Carlo Pucillo verfasserin aut Antonella De Luca verfasserin aut Emilia Nunzi verfasserin aut Roberta Spaccapelo verfasserin aut Marilena Pariano verfasserin aut Monica Borghi verfasserin aut Francesca Boscaro verfasserin aut Riccardo Romoli verfasserin aut Andrea Mancini verfasserin aut Lucia Gentili verfasserin aut Giorgia Renga verfasserin aut Claudio Costantini verfasserin aut Matteo Puccetti verfasserin aut Stefano Giovagnoli verfasserin aut Maurizio Ricci verfasserin aut Martina Antonini verfasserin aut Paolo Calabresi verfasserin aut Paolo Puccetti verfasserin aut Massimiliano Di Filippo verfasserin aut Luigina Romani verfasserin aut In Scientific Reports Nature Portfolio, 2011 14(2024), 1, Seite 16 (DE-627)663366712 (DE-600)2615211-3 20452322 nnns volume:14 year:2024 number:1 pages:16 https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/article/ef3dd28764624aada7153b8839b12acc kostenfrei https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/toc/2045-2322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2024 1 16 |
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10.1038/s41598-024-57400-8 doi (DE-627)DOAJ095739025 (DE-599)DOAJef3dd28764624aada7153b8839b12acc DE-627 ger DE-627 rakwb eng Teresa Zelante verfasserin aut A microbially produced AhR ligand promotes a Tph1-driven tolerogenic program in multiple sclerosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. Mast cells Aryl hydrocarbon receptor Serotonin 3-IAld Multiple sclerosis Medicine R Science Q Giuseppe Paolicelli verfasserin aut Francesca Fallarino verfasserin aut Marco Gargaro verfasserin aut Gianluca Vascelli verfasserin aut Marco De Zuani verfasserin aut Jan Fric verfasserin aut Petra Laznickova verfasserin aut Marcela Hortova Kohoutkova verfasserin aut Antonio Macchiarulo verfasserin aut Daniela Dolciami verfasserin aut Giuseppe Pieraccini verfasserin aut Lorenzo Gaetani verfasserin aut Giulia Scalisi verfasserin aut Caterina Trevisan verfasserin aut Barbara Frossi verfasserin aut Carlo Pucillo verfasserin aut Antonella De Luca verfasserin aut Emilia Nunzi verfasserin aut Roberta Spaccapelo verfasserin aut Marilena Pariano verfasserin aut Monica Borghi verfasserin aut Francesca Boscaro verfasserin aut Riccardo Romoli verfasserin aut Andrea Mancini verfasserin aut Lucia Gentili verfasserin aut Giorgia Renga verfasserin aut Claudio Costantini verfasserin aut Matteo Puccetti verfasserin aut Stefano Giovagnoli verfasserin aut Maurizio Ricci verfasserin aut Martina Antonini verfasserin aut Paolo Calabresi verfasserin aut Paolo Puccetti verfasserin aut Massimiliano Di Filippo verfasserin aut Luigina Romani verfasserin aut In Scientific Reports Nature Portfolio, 2011 14(2024), 1, Seite 16 (DE-627)663366712 (DE-600)2615211-3 20452322 nnns volume:14 year:2024 number:1 pages:16 https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/article/ef3dd28764624aada7153b8839b12acc kostenfrei https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/toc/2045-2322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2024 1 16 |
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10.1038/s41598-024-57400-8 doi (DE-627)DOAJ095739025 (DE-599)DOAJef3dd28764624aada7153b8839b12acc DE-627 ger DE-627 rakwb eng Teresa Zelante verfasserin aut A microbially produced AhR ligand promotes a Tph1-driven tolerogenic program in multiple sclerosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. Mast cells Aryl hydrocarbon receptor Serotonin 3-IAld Multiple sclerosis Medicine R Science Q Giuseppe Paolicelli verfasserin aut Francesca Fallarino verfasserin aut Marco Gargaro verfasserin aut Gianluca Vascelli verfasserin aut Marco De Zuani verfasserin aut Jan Fric verfasserin aut Petra Laznickova verfasserin aut Marcela Hortova Kohoutkova verfasserin aut Antonio Macchiarulo verfasserin aut Daniela Dolciami verfasserin aut Giuseppe Pieraccini verfasserin aut Lorenzo Gaetani verfasserin aut Giulia Scalisi verfasserin aut Caterina Trevisan verfasserin aut Barbara Frossi verfasserin aut Carlo Pucillo verfasserin aut Antonella De Luca verfasserin aut Emilia Nunzi verfasserin aut Roberta Spaccapelo verfasserin aut Marilena Pariano verfasserin aut Monica Borghi verfasserin aut Francesca Boscaro verfasserin aut Riccardo Romoli verfasserin aut Andrea Mancini verfasserin aut Lucia Gentili verfasserin aut Giorgia Renga verfasserin aut Claudio Costantini verfasserin aut Matteo Puccetti verfasserin aut Stefano Giovagnoli verfasserin aut Maurizio Ricci verfasserin aut Martina Antonini verfasserin aut Paolo Calabresi verfasserin aut Paolo Puccetti verfasserin aut Massimiliano Di Filippo verfasserin aut Luigina Romani verfasserin aut In Scientific Reports Nature Portfolio, 2011 14(2024), 1, Seite 16 (DE-627)663366712 (DE-600)2615211-3 20452322 nnns volume:14 year:2024 number:1 pages:16 https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/article/ef3dd28764624aada7153b8839b12acc kostenfrei https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/toc/2045-2322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2024 1 16 |
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10.1038/s41598-024-57400-8 doi (DE-627)DOAJ095739025 (DE-599)DOAJef3dd28764624aada7153b8839b12acc DE-627 ger DE-627 rakwb eng Teresa Zelante verfasserin aut A microbially produced AhR ligand promotes a Tph1-driven tolerogenic program in multiple sclerosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. Mast cells Aryl hydrocarbon receptor Serotonin 3-IAld Multiple sclerosis Medicine R Science Q Giuseppe Paolicelli verfasserin aut Francesca Fallarino verfasserin aut Marco Gargaro verfasserin aut Gianluca Vascelli verfasserin aut Marco De Zuani verfasserin aut Jan Fric verfasserin aut Petra Laznickova verfasserin aut Marcela Hortova Kohoutkova verfasserin aut Antonio Macchiarulo verfasserin aut Daniela Dolciami verfasserin aut Giuseppe Pieraccini verfasserin aut Lorenzo Gaetani verfasserin aut Giulia Scalisi verfasserin aut Caterina Trevisan verfasserin aut Barbara Frossi verfasserin aut Carlo Pucillo verfasserin aut Antonella De Luca verfasserin aut Emilia Nunzi verfasserin aut Roberta Spaccapelo verfasserin aut Marilena Pariano verfasserin aut Monica Borghi verfasserin aut Francesca Boscaro verfasserin aut Riccardo Romoli verfasserin aut Andrea Mancini verfasserin aut Lucia Gentili verfasserin aut Giorgia Renga verfasserin aut Claudio Costantini verfasserin aut Matteo Puccetti verfasserin aut Stefano Giovagnoli verfasserin aut Maurizio Ricci verfasserin aut Martina Antonini verfasserin aut Paolo Calabresi verfasserin aut Paolo Puccetti verfasserin aut Massimiliano Di Filippo verfasserin aut Luigina Romani verfasserin aut In Scientific Reports Nature Portfolio, 2011 14(2024), 1, Seite 16 (DE-627)663366712 (DE-600)2615211-3 20452322 nnns volume:14 year:2024 number:1 pages:16 https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/article/ef3dd28764624aada7153b8839b12acc kostenfrei https://doi.org/10.1038/s41598-024-57400-8 kostenfrei https://doaj.org/toc/2045-2322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2024 1 16 |
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Teresa Zelante @@aut@@ Giuseppe Paolicelli @@aut@@ Francesca Fallarino @@aut@@ Marco Gargaro @@aut@@ Gianluca Vascelli @@aut@@ Marco De Zuani @@aut@@ Jan Fric @@aut@@ Petra Laznickova @@aut@@ Marcela Hortova Kohoutkova @@aut@@ Antonio Macchiarulo @@aut@@ Daniela Dolciami @@aut@@ Giuseppe Pieraccini @@aut@@ Lorenzo Gaetani @@aut@@ Giulia Scalisi @@aut@@ Caterina Trevisan @@aut@@ Barbara Frossi @@aut@@ Carlo Pucillo @@aut@@ Antonella De Luca @@aut@@ Emilia Nunzi @@aut@@ Roberta Spaccapelo @@aut@@ Marilena Pariano @@aut@@ Monica Borghi @@aut@@ Francesca Boscaro @@aut@@ Riccardo Romoli @@aut@@ Andrea Mancini @@aut@@ Lucia Gentili @@aut@@ Giorgia Renga @@aut@@ Claudio Costantini @@aut@@ Matteo Puccetti @@aut@@ Stefano Giovagnoli @@aut@@ Maurizio Ricci @@aut@@ Martina Antonini @@aut@@ Paolo Calabresi @@aut@@ Paolo Puccetti @@aut@@ Massimiliano Di Filippo @@aut@@ Luigina Romani @@aut@@ |
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A microbially produced AhR ligand promotes a Tph1-driven tolerogenic program in multiple sclerosis Mast cells Aryl hydrocarbon receptor Serotonin 3-IAld Multiple sclerosis |
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A microbially produced AhR ligand promotes a Tph1-driven tolerogenic program in multiple sclerosis |
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Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. |
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Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. |
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Abstract Multiple sclerosis is a debilitating autoimmune disease, characterized by chronic inflammation of the central nervous system. While the significance of the gut microbiome on multiple sclerosis pathogenesis is established, the underlining mechanisms are unknown. We found that serum levels of the microbial postbiotic tryptophan metabolite indole-3-carboxaldehyde (3-IAld) inversely correlated with disease duration in multiple sclerosis patients. Much like the host-derived tryptophan derivative l-Kynurenine, 3-IAld would bind and activate the Aryl hydrocarbon Receptor (AhR), which, in turn, controls endogenous tryptophan catabolic pathways. As a result, in peripheral lymph nodes, microbial 3-IAld, affected mast-cell tryptophan metabolism, forcing mast cells to produce serotonin via Tph1. We thus propose a protective role for AhR–mast-cell activation driven by the microbiome, whereby natural metabolites or postbiotics will have a physiological role in immune homeostasis and may act as therapeutic targets in autoimmune diseases. |
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