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NPJ Biofilms Microbiomes
. 2024 Aug 1;10(1):66.
doi: 10.1038/s41522-024-00538-0. Gut microbiota dysbiosis is associated with altered tryptophan metabolism and dysregulated inflammatory response in COVID-19
Morgan Essex # 1 2 3 , Belén Millet Pascual-Leone # 4 , Ulrike Löber 1 2 3 , Mathias Kuhring 2 5 6 , Bowen Zhang 7 8 9 , Ulrike Brüning 5 , Raphaela Fritsche-Guenther 5 , Marta Krzanowski 4 , Facundo Fiocca Vernengo 4 , Sophia Brumhard 4 , Ivo Röwekamp 4 , Agata Anna Bielecka 10 11 , Till Robin Lesker 10 , Emanuel Wyler 12 , Markus Landthaler 12 13 , Andrej Mantei 14 , Christian Meisel 14 15 , Sandra Caesar 4 , Charlotte Thibeault 4 , Victor M Corman 14 16 17 , Lajos Marko 1 2 3 18 , Norbert Suttorp 4 19 , Till Strowig 7 10 11 , Florian Kurth 4 , Leif E Sander 4 19 , Yang Li 7 8 , Jennifer A Kirwan 2 5 20 , Sofia K Forslund 1 2 3 18 21 , Bastian Opitz 22 23 24
Affiliations
The clinical course of COVID-19 is variable and often unpredictable. To test the hypothesis that disease progression and inflammatory responses associate with alterations in the microbiome and metabolome, we analyzed metagenome, metabolome, cytokine, and transcriptome profiles of repeated samples from hospitalized COVID-19 patients and uninfected controls, and leveraged clinical information and post-hoc confounder analysis. Severe COVID-19 was associated with a depletion of beneficial intestinal microbes, whereas oropharyngeal microbiota disturbance was mainly linked to antibiotic use. COVID-19 severity was also associated with enhanced plasma concentrations of kynurenine and reduced levels of several other tryptophan metabolites, lysophosphatidylcholines, and secondary bile acids. Moreover, reduced concentrations of various tryptophan metabolites were associated with depletion of Faecalibacterium, and tryptophan decrease and kynurenine increase were linked to enhanced production of inflammatory cytokines. Collectively, our study identifies correlated microbiome and metabolome alterations as a potential contributor to inflammatory dysregulation in severe COVID-19.
. 2024 Aug 1;10(1):66.
doi: 10.1038/s41522-024-00538-0. Gut microbiota dysbiosis is associated with altered tryptophan metabolism and dysregulated inflammatory response in COVID-19
Morgan Essex # 1 2 3 , Belén Millet Pascual-Leone # 4 , Ulrike Löber 1 2 3 , Mathias Kuhring 2 5 6 , Bowen Zhang 7 8 9 , Ulrike Brüning 5 , Raphaela Fritsche-Guenther 5 , Marta Krzanowski 4 , Facundo Fiocca Vernengo 4 , Sophia Brumhard 4 , Ivo Röwekamp 4 , Agata Anna Bielecka 10 11 , Till Robin Lesker 10 , Emanuel Wyler 12 , Markus Landthaler 12 13 , Andrej Mantei 14 , Christian Meisel 14 15 , Sandra Caesar 4 , Charlotte Thibeault 4 , Victor M Corman 14 16 17 , Lajos Marko 1 2 3 18 , Norbert Suttorp 4 19 , Till Strowig 7 10 11 , Florian Kurth 4 , Leif E Sander 4 19 , Yang Li 7 8 , Jennifer A Kirwan 2 5 20 , Sofia K Forslund 1 2 3 18 21 , Bastian Opitz 22 23 24
Affiliations
- PMID: 39085233
- DOI: 10.1038/s41522-024-00538-0
The clinical course of COVID-19 is variable and often unpredictable. To test the hypothesis that disease progression and inflammatory responses associate with alterations in the microbiome and metabolome, we analyzed metagenome, metabolome, cytokine, and transcriptome profiles of repeated samples from hospitalized COVID-19 patients and uninfected controls, and leveraged clinical information and post-hoc confounder analysis. Severe COVID-19 was associated with a depletion of beneficial intestinal microbes, whereas oropharyngeal microbiota disturbance was mainly linked to antibiotic use. COVID-19 severity was also associated with enhanced plasma concentrations of kynurenine and reduced levels of several other tryptophan metabolites, lysophosphatidylcholines, and secondary bile acids. Moreover, reduced concentrations of various tryptophan metabolites were associated with depletion of Faecalibacterium, and tryptophan decrease and kynurenine increase were linked to enhanced production of inflammatory cytokines. Collectively, our study identifies correlated microbiome and metabolome alterations as a potential contributor to inflammatory dysregulation in severe COVID-19.