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16 results on '"Galleron, Nathalie"'

1. Alteration of Gut Microbiome in Patients With Schizophrenia Indicates Links Between Bacterial Tyrosine Biosynthesis and Cognitive Dysfunction

Author

Thirion, Florence, Speyer, Helene, Hansen, Tue Haldor, Nielsen, Trine, Fan, Yong, Le Chatelier, Emmanuelle, Fromentin, Sébastien, Berland, Magali, Plaza Oñate, Florian, Pons, Nicolas, Galleron, Nathalie, Levenez, Florence, Markó, Lajos, Birkner, Till, Jørgensen, Torben, Forslund, Sofia K., Vestergaard, Henrik, Hansen, Torben, Nordentoft, Merete, Mors, Ole, Benros, Michael E., Pedersen, Oluf, Ehrlich, Stanislav D., Thirion, Florence, Speyer, Helene, Hansen, Tue Haldor, Nielsen, Trine, Fan, Yong, Le Chatelier, Emmanuelle, Fromentin, Sébastien, Berland, Magali, Plaza Oñate, Florian, Pons, Nicolas, Galleron, Nathalie, Levenez, Florence, Markó, Lajos, Birkner, Till, Jørgensen, Torben, Forslund, Sofia K., Vestergaard, Henrik, Hansen, Torben, Nordentoft, Merete, Mors, Ole, Benros, Michael E., Pedersen, Oluf, and Ehrlich, Stanislav D.

Published
2023

2. Alteration of Gut Microbiome in Patients With Schizophrenia Indicates Links Between Bacterial Tyrosine Biosynthesis and Cognitive Dysfunction

Author

Thirion, Florence, Speyer, Helene, Hansen, Tue Haldor, Nielsen, Trine, Fan, Yong, Le Chatelier, Emmanuelle, Fromentin, Sébastien, Berland, Magali, Plaza Oñate, Florian, Pons, Nicolas, Galleron, Nathalie, Levenez, Florence, Markó, Lajos, Birkner, Till, Jørgensen, Torben, Forslund, Sofia K., Vestergaard, Henrik, Hansen, Torben, Nordentoft, Merete, Mors, Ole, Benros, Michael E., Pedersen, Oluf, Ehrlich, Stanislav D., Thirion, Florence, Speyer, Helene, Hansen, Tue Haldor, Nielsen, Trine, Fan, Yong, Le Chatelier, Emmanuelle, Fromentin, Sébastien, Berland, Magali, Plaza Oñate, Florian, Pons, Nicolas, Galleron, Nathalie, Levenez, Florence, Markó, Lajos, Birkner, Till, Jørgensen, Torben, Forslund, Sofia K., Vestergaard, Henrik, Hansen, Torben, Nordentoft, Merete, Mors, Ole, Benros, Michael E., Pedersen, Oluf, and Ehrlich, Stanislav D.

Published
2023

3. The gut microbiota contributes to the pathogenesis of anorexia nervosa in humans and mice

Author

Fan, Yong, Støving, René Klinkby, Berreira Ibraim, Samar, Hyötyläinen, Tuulia, Thirion, Florence, Arora, Tulika, Lyu, Liwei, Stankevic, Evelina, Hansen, Tue Haldor, Déchelotte, Pierre, Sinioja, Tim, Ragnarsdottir, Oddny, Pons, Nicolas, Galleron, Nathalie, Quinquis, Benoît, Levenez, Florence, Roume, Hugo, Falony, Gwen, Vieira-Silva, Sara, Raes, Jeroen, Clausen, Loa, Telléus, Gry Kjaersdam, Bäckhed, Fredrik, Oresic, Matej, Ehrlich, S. Dusko, Pedersen, Oluf, Fan, Yong, Støving, René Klinkby, Berreira Ibraim, Samar, Hyötyläinen, Tuulia, Thirion, Florence, Arora, Tulika, Lyu, Liwei, Stankevic, Evelina, Hansen, Tue Haldor, Déchelotte, Pierre, Sinioja, Tim, Ragnarsdottir, Oddny, Pons, Nicolas, Galleron, Nathalie, Quinquis, Benoît, Levenez, Florence, Roume, Hugo, Falony, Gwen, Vieira-Silva, Sara, Raes, Jeroen, Clausen, Loa, Telléus, Gry Kjaersdam, Bäckhed, Fredrik, Oresic, Matej, Ehrlich, S. Dusko, and Pedersen, Oluf

Abstract

Anorexia nervosa (AN) is an eating disorder with a high mortality. About 95% of cases are women and it has a population prevalence of about 1%, but evidence-based treatment is lacking. The pathogenesis of AN probably involves genetics and various environmental factors, and an altered gut microbiota has been observed in individuals with AN using amplicon sequencing and relatively small cohorts. Here we investigated whether a disrupted gut microbiota contributes to AN pathogenesis. Shotgun metagenomics and metabolomics were performed on faecal and serum samples, respectively, from a cohort of 77 females with AN and 70 healthy females. Multiple bacterial taxa (for example, Clostridium species) were altered in AN and correlated with estimates of eating behaviour and mental health. The gut virome was also altered in AN including a reduction in viral-bacterial interactions. Bacterial functional modules associated with the degradation of neurotransmitters were enriched in AN and various structural variants in bacteria were linked to metabolic features of AN. Serum metabolomics revealed an increase in metabolites associated with reduced food intake (for example, indole-3-propionic acid). Causal inference analyses implied that serum bacterial metabolites are potentially mediating the impact of an altered gut microbiota on AN behaviour. Further, we performed faecal microbiota transplantation from AN cases to germ-free mice under energy-restricted feeding to mirror AN eating behaviour. We found that the reduced weight gain and induced hypothalamic and adipose tissue gene expression were related to aberrant energy metabolism and eating behaviour. Our 'omics' and mechanistic studies imply that a disruptive gut microbiome may contribute to AN pathogenesis., Funding agencies:Marie Sklodowska-Curie Individual Fellowship 797267Odense University Hospital Research Fund R15-A800

Published
2023
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4. The gut microbiota contributes to the pathogenesis of anorexia nervosa in humans and mice

Author

Fan, Yong, Støving, René Klinkby, Berreira Ibraim, Samar, Hyötyläinen, Tuulia, Thirion, Florence, Arora, Tulika, Lyu, Liwei, Stankevic, Evelina, Hansen, Tue Haldor, Déchelotte, Pierre, Sinioja, Tim, Ragnarsdottir, Oddny, Pons, Nicolas, Galleron, Nathalie, Quinquis, Benoît, Levenez, Florence, Roume, Hugo, Falony, Gwen, Vieira-Silva, Sara, Raes, Jeroen, Clausen, Loa, Telléus, Gry Kjaersdam, Bäckhed, Fredrik, Oresic, Matej, Ehrlich, S. Dusko, Pedersen, Oluf, Fan, Yong, Støving, René Klinkby, Berreira Ibraim, Samar, Hyötyläinen, Tuulia, Thirion, Florence, Arora, Tulika, Lyu, Liwei, Stankevic, Evelina, Hansen, Tue Haldor, Déchelotte, Pierre, Sinioja, Tim, Ragnarsdottir, Oddny, Pons, Nicolas, Galleron, Nathalie, Quinquis, Benoît, Levenez, Florence, Roume, Hugo, Falony, Gwen, Vieira-Silva, Sara, Raes, Jeroen, Clausen, Loa, Telléus, Gry Kjaersdam, Bäckhed, Fredrik, Oresic, Matej, Ehrlich, S. Dusko, and Pedersen, Oluf

Abstract

Anorexia nervosa (AN) is an eating disorder with a high mortality. About 95% of cases are women and it has a population prevalence of about 1%, but evidence-based treatment is lacking. The pathogenesis of AN probably involves genetics and various environmental factors, and an altered gut microbiota has been observed in individuals with AN using amplicon sequencing and relatively small cohorts. Here we investigated whether a disrupted gut microbiota contributes to AN pathogenesis. Shotgun metagenomics and metabolomics were performed on faecal and serum samples, respectively, from a cohort of 77 females with AN and 70 healthy females. Multiple bacterial taxa (for example, Clostridium species) were altered in AN and correlated with estimates of eating behaviour and mental health. The gut virome was also altered in AN including a reduction in viral–bacterial interactions. Bacterial functional modules associated with the degradation of neurotransmitters were enriched in AN and various structural variants in bacteria were linked to metabolic features of AN. Serum metabolomics revealed an increase in metabolites associated with reduced food intake (for example, indole-3-propionic acid). Causal inference analyses implied that serum bacterial metabolites are potentially mediating the impact of an altered gut microbiota on AN behaviour. Further, we performed faecal microbiota transplantation from AN cases to germ-free mice under energy-restricted feeding to mirror AN eating behaviour. We found that the reduced weight gain and induced hypothalamic and adipose tissue gene expression were related to aberrant energy metabolism and eating behaviour. Our ‘omics’ and mechanistic studies imply that a disruptive gut microbiome may contribute to AN pathogenesis.

Published
2023

5. The gut microbiota contributes to the pathogenesis of anorexia nervosa in humans and mice

Author

Fan, Yong, Støving, René Klinkby, Berreira Ibraim, Samar, Hyötyläinen, Tuulia, Thirion, Florence, Arora, Tulika, Lyu, Liwei, Stankevic, Evelina, Hansen, Tue Haldor, Déchelotte, Pierre, Sinioja, Tim, Ragnarsdottir, Oddny, Pons, Nicolas, Galleron, Nathalie, Quinquis, Benoît, Levenez, Florence, Roume, Hugo, Falony, Gwen, Vieira-Silva, Sara, Raes, Jeroen, Clausen, Loa, Telléus, Gry Kjaersdam, Bäckhed, Fredrik, Oresic, Matej, Ehrlich, S. Dusko, Pedersen, Oluf, Fan, Yong, Støving, René Klinkby, Berreira Ibraim, Samar, Hyötyläinen, Tuulia, Thirion, Florence, Arora, Tulika, Lyu, Liwei, Stankevic, Evelina, Hansen, Tue Haldor, Déchelotte, Pierre, Sinioja, Tim, Ragnarsdottir, Oddny, Pons, Nicolas, Galleron, Nathalie, Quinquis, Benoît, Levenez, Florence, Roume, Hugo, Falony, Gwen, Vieira-Silva, Sara, Raes, Jeroen, Clausen, Loa, Telléus, Gry Kjaersdam, Bäckhed, Fredrik, Oresic, Matej, Ehrlich, S. Dusko, and Pedersen, Oluf

Abstract

Anorexia nervosa (AN) is an eating disorder with a high mortality. About 95% of cases are women and it has a population prevalence of about 1%, but evidence-based treatment is lacking. The pathogenesis of AN probably involves genetics and various environmental factors, and an altered gut microbiota has been observed in individuals with AN using amplicon sequencing and relatively small cohorts. Here we investigated whether a disrupted gut microbiota contributes to AN pathogenesis. Shotgun metagenomics and metabolomics were performed on faecal and serum samples, respectively, from a cohort of 77 females with AN and 70 healthy females. Multiple bacterial taxa (for example, Clostridium species) were altered in AN and correlated with estimates of eating behaviour and mental health. The gut virome was also altered in AN including a reduction in viral–bacterial interactions. Bacterial functional modules associated with the degradation of neurotransmitters were enriched in AN and various structural variants in bacteria were linked to metabolic features of AN. Serum metabolomics revealed an increase in metabolites associated with reduced food intake (for example, indole-3-propionic acid). Causal inference analyses implied that serum bacterial metabolites are potentially mediating the impact of an altered gut microbiota on AN behaviour. Further, we performed faecal microbiota transplantation from AN cases to germ-free mice under energy-restricted feeding to mirror AN eating behaviour. We found that the reduced weight gain and induced hypothalamic and adipose tissue gene expression were related to aberrant energy metabolism and eating behaviour. Our ‘omics’ and mechanistic studies imply that a disruptive gut microbiome may contribute to AN pathogenesis.

Published
2023

6. Impairment of gut microbial biotin metabolism and host biotin status in severe obesity: effect of biotin and prebiotic supplementation on improved metabolism

Author

Belda, Eugeni, Voland, Lise, Tremaroli, Valentina, Falony, Gwen, Adriouch, Solia, Assmann, Karen E., Prifti, Edi, Aron-Wisnewsky, Judith, Debédat, Jean, Le Roy, Tiphaine, Nielsen, Trine, Amouya, Chloé, André, Sébastien, Andreelli,, Fabrizio, Blüher, Matthias Blüher, Chakaroun, Rima, Chilloux, Julien, Coelho, Luis Pedro, Dao, Maria Carlota, Das, Promi, Fellahi, Soraya, Forslund, Sofia, Galleron, Nathalie, Hansen, Tue, Holmes, Bridget, Ji, Boyang, Krogh Pedersen, Helle, Le, Phuong, Le Chatelier, Emmanuelle, Lewinter, Christian, Mannerås-Holm, Louise, Marquet, Florian, Myridakis, Antonis, Pelloux, Veronique, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Sokolovska, Nataliya, Søndertoft, Nadja B, Touch, Sothea, Vieira-Silva, Sara, Consortium, MetaCardis, Galan, Pilar, Holst, Jens, Gøtze, Jens Peter, Køber, Lars, Vestergaard, Henrik, Hansen, Torben, Hercberg, Serge, Oppert, Jean-Michel, Nielsen, Jens, Letunic, Ivica, Dumas, Marc-Emmanuel, Stumvol, Michael, Pedersen, Oluf Borbye, Bork, Peer, Dusko Ehrlich, Stanislav, Zucker, Jens-Daniel, Bäckhed, Fredrik, Raes, Jeroen, Clément, Karine, Belda, Eugeni, Voland, Lise, Tremaroli, Valentina, Falony, Gwen, Adriouch, Solia, Assmann, Karen E., Prifti, Edi, Aron-Wisnewsky, Judith, Debédat, Jean, Le Roy, Tiphaine, Nielsen, Trine, Amouya, Chloé, André, Sébastien, Andreelli,, Fabrizio, Blüher, Matthias Blüher, Chakaroun, Rima, Chilloux, Julien, Coelho, Luis Pedro, Dao, Maria Carlota, Das, Promi, Fellahi, Soraya, Forslund, Sofia, Galleron, Nathalie, Hansen, Tue, Holmes, Bridget, Ji, Boyang, Krogh Pedersen, Helle, Le, Phuong, Le Chatelier, Emmanuelle, Lewinter, Christian, Mannerås-Holm, Louise, Marquet, Florian, Myridakis, Antonis, Pelloux, Veronique, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Sokolovska, Nataliya, Søndertoft, Nadja B, Touch, Sothea, Vieira-Silva, Sara, Consortium, MetaCardis, Galan, Pilar, Holst, Jens, Gøtze, Jens Peter, Køber, Lars, Vestergaard, Henrik, Hansen, Torben, Hercberg, Serge, Oppert, Jean-Michel, Nielsen, Jens, Letunic, Ivica, Dumas, Marc-Emmanuel, Stumvol, Michael, Pedersen, Oluf Borbye, Bork, Peer, Dusko Ehrlich, Stanislav, Zucker, Jens-Daniel, Bäckhed, Fredrik, Raes, Jeroen, and Clément, Karine

Abstract

Gut microbiota is a key component in obesity and type 2 diabetes, yet mechanisms and metabolites central to this interaction remain unclear. We examined the human gut microbiome’s functional composition in healthy metabolic state and the most severe states of obesity and type 2 diabetes within the MetaCardis cohort. We focused on the role of B vitamins and B7/B8 biotin for regulation of host metabolic state, as these vitamins influence both microbial function and host metabolism and inflammation.

Published
2022

7. Impairment of gut microbial biotin metabolism and host biotin status in severe obesity: effect of biotin and prebiotic supplementation on improved metabolism

Author

Belda, Eugeni, Voland, Lise, Tremaroli, Valentina, Falony, Gwen, Adriouch, Solia, Assmann, Karen E., Prifti, Edi, Aron-Wisnewsky, Judith, Debédat, Jean, Le Roy, Tiphaine, Nielsen, Trine, Amouya, Chloé, André, Sébastien, Andreelli,, Fabrizio, Blüher, Matthias Blüher, Chakaroun, Rima, Chilloux, Julien, Coelho, Luis Pedro, Dao, Maria Carlota, Das, Promi, Fellahi, Soraya, Forslund, Sofia, Galleron, Nathalie, Hansen, Tue, Holmes, Bridget, Ji, Boyang, Krogh Pedersen, Helle, Le, Phuong, Le Chatelier, Emmanuelle, Lewinter, Christian, Mannerås-Holm, Louise, Marquet, Florian, Myridakis, Antonis, Pelloux, Veronique, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Sokolovska, Nataliya, Søndertoft, Nadja B, Touch, Sothea, Vieira-Silva, Sara, Consortium, MetaCardis, Galan, Pilar, Holst, Jens, Gøtze, Jens Peter, Køber, Lars, Vestergaard, Henrik, Hansen, Torben, Hercberg, Serge, Oppert, Jean-Michel, Nielsen, Jens, Letunic, Ivica, Dumas, Marc-Emmanuel, Stumvol, Michael, Pedersen, Oluf Borbye, Bork, Peer, Dusko Ehrlich, Stanislav, Zucker, Jens-Daniel, Bäckhed, Fredrik, Raes, Jeroen, Clément, Karine, Belda, Eugeni, Voland, Lise, Tremaroli, Valentina, Falony, Gwen, Adriouch, Solia, Assmann, Karen E., Prifti, Edi, Aron-Wisnewsky, Judith, Debédat, Jean, Le Roy, Tiphaine, Nielsen, Trine, Amouya, Chloé, André, Sébastien, Andreelli,, Fabrizio, Blüher, Matthias Blüher, Chakaroun, Rima, Chilloux, Julien, Coelho, Luis Pedro, Dao, Maria Carlota, Das, Promi, Fellahi, Soraya, Forslund, Sofia, Galleron, Nathalie, Hansen, Tue, Holmes, Bridget, Ji, Boyang, Krogh Pedersen, Helle, Le, Phuong, Le Chatelier, Emmanuelle, Lewinter, Christian, Mannerås-Holm, Louise, Marquet, Florian, Myridakis, Antonis, Pelloux, Veronique, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Sokolovska, Nataliya, Søndertoft, Nadja B, Touch, Sothea, Vieira-Silva, Sara, Consortium, MetaCardis, Galan, Pilar, Holst, Jens, Gøtze, Jens Peter, Køber, Lars, Vestergaard, Henrik, Hansen, Torben, Hercberg, Serge, Oppert, Jean-Michel, Nielsen, Jens, Letunic, Ivica, Dumas, Marc-Emmanuel, Stumvol, Michael, Pedersen, Oluf Borbye, Bork, Peer, Dusko Ehrlich, Stanislav, Zucker, Jens-Daniel, Bäckhed, Fredrik, Raes, Jeroen, and Clément, Karine

Abstract

Gut microbiota is a key component in obesity and type 2 diabetes, yet mechanisms and metabolites central to this interaction remain unclear. We examined the human gut microbiome’s functional composition in healthy metabolic state and the most severe states of obesity and type 2 diabetes within the MetaCardis cohort. We focused on the role of B vitamins and B7/B8 biotin for regulation of host metabolic state, as these vitamins influence both microbial function and host metabolism and inflammation.

Published
2022

8. Rifaximin-alpha reduces gut-derived inflammation and mucin degradation in cirrhosis and encephalopathy : RIFSYS randomised controlled trial

Author

Patel, Vishal C., Lee, Sunjae, McPhail, Mark J. W., Da Silva, Kevin, Guilly, Susie, Zamalloa, Ane, Witherden, Elizabeth, Stoy, Sidsel, Vijay, Godhev Kumar Manakkat, Pons, Nicolas, Galleron, Nathalie, Huang, Xaiohong, Gencer, Selin, Coen, Muireann, Tranah, Thomas Henry, Wendon, Julia Alexis, Bruce, Kenneth D., Le Chatelier, Emmanuelle, Ehrlich, Stanislav Dusko, Edwards, Lindsey Ann, Shoaie, Saeed, Shawcross, Debbie Lindsay, Patel, Vishal C., Lee, Sunjae, McPhail, Mark J. W., Da Silva, Kevin, Guilly, Susie, Zamalloa, Ane, Witherden, Elizabeth, Stoy, Sidsel, Vijay, Godhev Kumar Manakkat, Pons, Nicolas, Galleron, Nathalie, Huang, Xaiohong, Gencer, Selin, Coen, Muireann, Tranah, Thomas Henry, Wendon, Julia Alexis, Bruce, Kenneth D., Le Chatelier, Emmanuelle, Ehrlich, Stanislav Dusko, Edwards, Lindsey Ann, Shoaie, Saeed, and Shawcross, Debbie Lindsay

Abstract

Background & Aims: Rifaximin-alpha is efficacious for the prevention of recurrent hepatic encephalopathy (HE), but its mechanism of action remains unclear. We postulated that rifaximin-alpha reduces gut microbiota-derived endotoxemia and systemic inflammation, a known driver of HE. Methods: In a placebo-controlled, double-blind, mechanistic study, 38 patients with cirrhosis and HE were randomised 1:1 to receive either rifaximin-alpha (550 mg BID) or placebo for 90 days. Primary outcome: 50% reduction in neutrophil oxidative burst (OB) at 30 days. Secondary outcomes: changes in psychometric hepatic encephalopathy score (PHES) and neurocognitive functioning, shotgun metagenomic sequencing of saliva and faeces, plasma and faecal metabolic profiling, whole blood bacterial DNA quantification, neutrophil toll-like receptor (TLR)-2/4/9 expression and plasma/faecal cytokine analysis. Results: Patients were well-matched: median MELD (11 rifaximin-alpha vs. 10 placebo). Rifaximin-alpha did not lead to a 50% reduction in spontaneous neutrophil OB at 30 days compared to baseline (p = 0.48). However, HE grade normalised (p = 0.014) and PHES improved (p = 0.009) after 30 days on rifaximin-alpha. Rifaximin-alpha reduced circulating neutrophil TLR-4 expression on day 30 (p = 0.021) and plasma tumour necrosis factor-alpha (TNF-alpha) (p <0.001). Rifaximin-a suppressed oralisation of the gut, reducing levels of mucin-degrading sialidase-rich species, Streptococcus spp, Veillonella atypica and parvula, Akkermansia and Hungatella. Rifaximin-alpha promoted a TNF-alpha-and interleukin17E-enriched intestinal microenvironment, augmenting antibacterial responses to invading pathobionts and promoting gut barrier repair. Those on rifaximin-alpha were less likely to develop infection (odds ratio 0.21; 95% CI 0.05-0.96). Conclusion: Rifaximin-alpha led to resolution of overt and covert HE, reduced the likelihood of infection, reduced oralisation of the gut and attenuated systemic inflamm, QC 20220304

Published
2022
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9. Impairment of gut microbial biotin metabolism and host biotin status in severe obesity:effect of biotin and prebiotic supplementation on improved metabolism

Author

Belda, Eugeni, Voland, Lise, Tremaroli, Valentina, Falony, Gwen, Adriouch, Solia, Assmann, Karen E., Prifiti, Edi, Aron-Wisnewsky, Judith, Debedat, Jean, Le Roy, Tiphaine, Nielsen, Trine, Amouyal, Chloe, Andre, Sebastien, Andreelli, Fabrizio, Blueher, Matthias, Chakaroun, Rima, Chilloux, Julien, Coelho, Luis Pedro, Dao, Maria Carlota, Das, Promi, Fellahi, Soraya, Forslund, Sofia, Galleron, Nathalie, Hansen, Tue H., Holmes, Bridget, Ji, Boyang, Pedersen, Helle Krogh, Phuong Le, Le Chatelier, Emmanuelle, Lewinter, Christian, Manneras-Holm, Louise, Marquet, Florian, Myridakis, Antonis, Pelloux, Veronique, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Sokolovska, Nataliya, Søndertoft, Nadja B., Touch, Sothea, Vieira-Silva, Sara, Galan, Pilar, Holst, Jens, Gøtze, Jens Peter, Køber, Lars, Vestergaard, Henrik, Hansen, Torben, Hercberg, Serge, Oppert, Jean-Michel, Nielsen, Jens, Letunic, Ivica, Dumas, Marc-Emmanuel, Stumvoll, Michael, Pedersen, Oluf Borbye, Bork, Peer, Ehrlich, Stanislav Dusko, Zucker, Jean-Daniel, Baeckhed, Fredrik, Raes, Jeroen, Clement, Karine, Belda, Eugeni, Voland, Lise, Tremaroli, Valentina, Falony, Gwen, Adriouch, Solia, Assmann, Karen E., Prifiti, Edi, Aron-Wisnewsky, Judith, Debedat, Jean, Le Roy, Tiphaine, Nielsen, Trine, Amouyal, Chloe, Andre, Sebastien, Andreelli, Fabrizio, Blueher, Matthias, Chakaroun, Rima, Chilloux, Julien, Coelho, Luis Pedro, Dao, Maria Carlota, Das, Promi, Fellahi, Soraya, Forslund, Sofia, Galleron, Nathalie, Hansen, Tue H., Holmes, Bridget, Ji, Boyang, Pedersen, Helle Krogh, Phuong Le, Le Chatelier, Emmanuelle, Lewinter, Christian, Manneras-Holm, Louise, Marquet, Florian, Myridakis, Antonis, Pelloux, Veronique, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Sokolovska, Nataliya, Søndertoft, Nadja B., Touch, Sothea, Vieira-Silva, Sara, Galan, Pilar, Holst, Jens, Gøtze, Jens Peter, Køber, Lars, Vestergaard, Henrik, Hansen, Torben, Hercberg, Serge, Oppert, Jean-Michel, Nielsen, Jens, Letunic, Ivica, Dumas, Marc-Emmanuel, Stumvoll, Michael, Pedersen, Oluf Borbye, Bork, Peer, Ehrlich, Stanislav Dusko, Zucker, Jean-Daniel, Baeckhed, Fredrik, Raes, Jeroen, and Clement, Karine

Published
2022

10. Microbiome and metabolome features of the cardiometabolic disease spectrum

Author

Fromentin, Sebastien, Forslund, Sofia K., Chechi, Kanta, Aron-Wisnewsky, Judith, Chakaroun, Rima, Nielsen, Trine, Tremaroli, Valentina, Ji, Boyang, Prifti, Edi, Myridakis, Antonis, Chilloux, Julien, Andrikopoulos, Petros, Fan, Yong, Olanipekun, Michael T., Alves, Renato, Adiouch, Solia, Bar, Noam, Talmor-Barkan, Yeela, Belda, Eugeni, Caesar, Robert, Coelho, Luis Pedro, Falony, Gwen, Fellahi, Soraya, Galan, Pilar, Galleron, Nathalie, Helft, Gerard, Hoyles, Lesley, Isnard, Richard, Le Chatelier, Emmanuelle, Julienne, Hanna, Olsson, Lisa, Pedersen, Helle Krogh, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe Elie, Schmidt, Thomas S.B., Vieira-Silva, Sara, Li, Peishun, Zimmermann-Kogadeeva, Maria, Lewinter, Christian, Søndertoft, Nadja B., Hansen, Tue H., Gauguier, Dominique, Gøtze, Jens Peter, Køber, Lars, Kornowski, Ran, Vestergaard, Henrik, Hansen, Torben, Zucker, Jean Daniel, Hercberg, Serge, Letunic, Ivica, Bäckhed, Fredrik, Oppert, Jean Michel, Nielsen, Jens, Raes, Jeroen, Bork, Peer, Stumvoll, Michael, Segal, Eran, Clément, Karine, Dumas, Marc Emmanuel, Ehrlich, S. Dusko, Pedersen, Oluf, Fromentin, Sebastien, Forslund, Sofia K., Chechi, Kanta, Aron-Wisnewsky, Judith, Chakaroun, Rima, Nielsen, Trine, Tremaroli, Valentina, Ji, Boyang, Prifti, Edi, Myridakis, Antonis, Chilloux, Julien, Andrikopoulos, Petros, Fan, Yong, Olanipekun, Michael T., Alves, Renato, Adiouch, Solia, Bar, Noam, Talmor-Barkan, Yeela, Belda, Eugeni, Caesar, Robert, Coelho, Luis Pedro, Falony, Gwen, Fellahi, Soraya, Galan, Pilar, Galleron, Nathalie, Helft, Gerard, Hoyles, Lesley, Isnard, Richard, Le Chatelier, Emmanuelle, Julienne, Hanna, Olsson, Lisa, Pedersen, Helle Krogh, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe Elie, Schmidt, Thomas S.B., Vieira-Silva, Sara, Li, Peishun, Zimmermann-Kogadeeva, Maria, Lewinter, Christian, Søndertoft, Nadja B., Hansen, Tue H., Gauguier, Dominique, Gøtze, Jens Peter, Køber, Lars, Kornowski, Ran, Vestergaard, Henrik, Hansen, Torben, Zucker, Jean Daniel, Hercberg, Serge, Letunic, Ivica, Bäckhed, Fredrik, Oppert, Jean Michel, Nielsen, Jens, Raes, Jeroen, Bork, Peer, Stumvoll, Michael, Segal, Eran, Clément, Karine, Dumas, Marc Emmanuel, Ehrlich, S. Dusko, and Pedersen, Oluf

Abstract

Previous microbiome and metabolome analyses exploring non-communicable diseases have paid scant attention to major confounders of study outcomes, such as common, pre-morbid and co-morbid conditions, or polypharmacy. Here, in the context of ischemic heart disease (IHD), we used a study design that recapitulates disease initiation, escalation and response to treatment over time, mirroring a longitudinal study that would otherwise be difficult to perform given the protracted nature of IHD pathogenesis. We recruited 1,241 middle-aged Europeans, including healthy individuals, individuals with dysmetabolic morbidities (obesity and type 2 diabetes) but lacking overt IHD diagnosis and individuals with IHD at three distinct clinical stages—acute coronary syndrome, chronic IHD and IHD with heart failure—and characterized their phenome, gut metagenome and serum and urine metabolome. We found that about 75% of microbiome and metabolome features that distinguish individuals with IHD from healthy individuals after adjustment for effects of medication and lifestyle are present in individuals exhibiting dysmetabolism, suggesting that major alterations of the gut microbiome and metabolome might begin long before clinical onset of IHD. We further categorized microbiome and metabolome signatures related to prodromal dysmetabolism, specific to IHD in general or to each of its three subtypes or related to escalation or de-escalation of IHD. Discriminant analysis based on specific IHD microbiome and metabolome features could better differentiate individuals with IHD from healthy individuals or metabolically matched individuals as compared to the conventional risk markers, pointing to a pathophysiological relevance of these features.

Published
2022

11. Microbiome and metabolome features of the cardiometabolic disease spectrum

Author

Fromentin, Sebastien, Forslund, Sofia K., Chechi, Kanta, Aron-Wisnewsky, Judith, Chakaroun, Rima, Nielsen, Trine, Tremaroli, Valentina, Ji, Boyang, Prifti, Edi, Myridakis, Antonis, Chilloux, Julien, Andrikopoulos, Petros, Fan, Yong, Olanipekun, Michael T., Alves, Renato, Adiouch, Solia, Bar, Noam, Talmor-Barkan, Yeela, Belda, Eugeni, Caesar, Robert, Coelho, Luis Pedro, Falony, Gwen, Fellahi, Soraya, Galan, Pilar, Galleron, Nathalie, Helft, Gerard, Hoyles, Lesley, Isnard, Richard, Le Chatelier, Emmanuelle, Julienne, Hanna, Olsson, Lisa, Pedersen, Helle Krogh, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe Elie, Schmidt, Thomas S.B., Vieira-Silva, Sara, Li, Peishun, Zimmermann-Kogadeeva, Maria, Lewinter, Christian, Søndertoft, Nadja B., Hansen, Tue H., Gauguier, Dominique, Gøtze, Jens Peter, Køber, Lars, Kornowski, Ran, Vestergaard, Henrik, Hansen, Torben, Zucker, Jean Daniel, Hercberg, Serge, Letunic, Ivica, Bäckhed, Fredrik, Oppert, Jean Michel, Nielsen, Jens, Raes, Jeroen, Bork, Peer, Stumvoll, Michael, Segal, Eran, Clément, Karine, Dumas, Marc Emmanuel, Ehrlich, S. Dusko, Pedersen, Oluf, Fromentin, Sebastien, Forslund, Sofia K., Chechi, Kanta, Aron-Wisnewsky, Judith, Chakaroun, Rima, Nielsen, Trine, Tremaroli, Valentina, Ji, Boyang, Prifti, Edi, Myridakis, Antonis, Chilloux, Julien, Andrikopoulos, Petros, Fan, Yong, Olanipekun, Michael T., Alves, Renato, Adiouch, Solia, Bar, Noam, Talmor-Barkan, Yeela, Belda, Eugeni, Caesar, Robert, Coelho, Luis Pedro, Falony, Gwen, Fellahi, Soraya, Galan, Pilar, Galleron, Nathalie, Helft, Gerard, Hoyles, Lesley, Isnard, Richard, Le Chatelier, Emmanuelle, Julienne, Hanna, Olsson, Lisa, Pedersen, Helle Krogh, Pons, Nicolas, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe Elie, Schmidt, Thomas S.B., Vieira-Silva, Sara, Li, Peishun, Zimmermann-Kogadeeva, Maria, Lewinter, Christian, Søndertoft, Nadja B., Hansen, Tue H., Gauguier, Dominique, Gøtze, Jens Peter, Køber, Lars, Kornowski, Ran, Vestergaard, Henrik, Hansen, Torben, Zucker, Jean Daniel, Hercberg, Serge, Letunic, Ivica, Bäckhed, Fredrik, Oppert, Jean Michel, Nielsen, Jens, Raes, Jeroen, Bork, Peer, Stumvoll, Michael, Segal, Eran, Clément, Karine, Dumas, Marc Emmanuel, Ehrlich, S. Dusko, and Pedersen, Oluf

Abstract

Previous microbiome and metabolome analyses exploring non-communicable diseases have paid scant attention to major confounders of study outcomes, such as common, pre-morbid and co-morbid conditions, or polypharmacy. Here, in the context of ischemic heart disease (IHD), we used a study design that recapitulates disease initiation, escalation and response to treatment over time, mirroring a longitudinal study that would otherwise be difficult to perform given the protracted nature of IHD pathogenesis. We recruited 1,241 middle-aged Europeans, including healthy individuals, individuals with dysmetabolic morbidities (obesity and type 2 diabetes) but lacking overt IHD diagnosis and individuals with IHD at three distinct clinical stages—acute coronary syndrome, chronic IHD and IHD with heart failure—and characterized their phenome, gut metagenome and serum and urine metabolome. We found that about 75% of microbiome and metabolome features that distinguish individuals with IHD from healthy individuals after adjustment for effects of medication and lifestyle are present in individuals exhibiting dysmetabolism, suggesting that major alterations of the gut microbiome and metabolome might begin long before clinical onset of IHD. We further categorized microbiome and metabolome signatures related to prodromal dysmetabolism, specific to IHD in general or to each of its three subtypes or related to escalation or de-escalation of IHD. Discriminant analysis based on specific IHD microbiome and metabolome features could better differentiate individuals with IHD from healthy individuals or metabolically matched individuals as compared to the conventional risk markers, pointing to a pathophysiological relevance of these features.

Published
2022

12. Combinatorial, additive and dose-dependent drug–microbiome associations

Author

Forslund, Sofia K., Chakaroun, Rima, Zimmermann-Kogadeeva, Maria, Markó, Lajos, Aron-Wisnewsky, Judith, Nielsen, Trine, Moitinho-Silva, Lucas, Schmidt, Thomas S.B., Falony, Gwen, Vieira-Silva, Sara, Adriouch, Solia, Alves, Renato J., Assmann, Karen, Bastard, Jean Philippe, Birkner, Till, Caesar, Robert, Chilloux, Julien, Coelho, Luis Pedro, Fezeu, Leopold, Galleron, Nathalie, Helft, Gerard, Isnard, Richard, Ji, Boyang, Kuhn, Michael, Le Chatelier, Emmanuelle, Myridakis, Antonis, Olsson, Lisa, Pons, Nicolas, Prifti, Edi, Quinquis, Benoit, Roume, Hugo, Lewinter, Christian, Søndertoft, Nadja B., Pedersen, Helle Krogh, Hansen, Tue H., Hartmann, Bolette, Holst, Jens Juul, Hornbak, Malene, Jørgensen, Niklas Rye, Justesen, Johanne, Krarup, Nikolaj, Svendstrup, Mathilde, Forslund, Sofia K., Chakaroun, Rima, Zimmermann-Kogadeeva, Maria, Markó, Lajos, Aron-Wisnewsky, Judith, Nielsen, Trine, Moitinho-Silva, Lucas, Schmidt, Thomas S.B., Falony, Gwen, Vieira-Silva, Sara, Adriouch, Solia, Alves, Renato J., Assmann, Karen, Bastard, Jean Philippe, Birkner, Till, Caesar, Robert, Chilloux, Julien, Coelho, Luis Pedro, Fezeu, Leopold, Galleron, Nathalie, Helft, Gerard, Isnard, Richard, Ji, Boyang, Kuhn, Michael, Le Chatelier, Emmanuelle, Myridakis, Antonis, Olsson, Lisa, Pons, Nicolas, Prifti, Edi, Quinquis, Benoit, Roume, Hugo, Lewinter, Christian, Søndertoft, Nadja B., Pedersen, Helle Krogh, Hansen, Tue H., Hartmann, Bolette, Holst, Jens Juul, Hornbak, Malene, Jørgensen, Niklas Rye, Justesen, Johanne, Krarup, Nikolaj, and Svendstrup, Mathilde

Abstract

During the transition from a healthy state to cardiometabolic disease, patients become heavily medicated, which leads to an increasingly aberrant gut microbiome and serum metabolome, and complicates biomarker discovery1–5. Here, through integrated multi-omics analyses of 2,173 European residents from the MetaCardis cohort, we show that the explanatory power of drugs for the variability in both host and gut microbiome features exceeds that of disease. We quantify inferred effects of single medications, their combinations as well as additive effects, and show that the latter shift the metabolome and microbiome towards a healthier state, exemplified in synergistic reduction in serum atherogenic lipoproteins by statins combined with aspirin, or enrichment of intestinal Roseburia by diuretic agents combined with beta-blockers. Several antibiotics exhibit a quantitative relationship between the number of courses prescribed and progression towards a microbiome state that is associated with the severity of cardiometabolic disease. We also report a relationship between cardiometabolic drug dosage, improvement in clinical markers and microbiome composition, supporting direct drug effects. Taken together, our computational framework and resulting resources enable the disentanglement of the effects of drugs and disease on host and microbiome features in multimedicated individuals. Furthermore, the robust signatures identified using our framework provide new hypotheses for drug–host–microbiome interactions in cardiometabolic disease.

Published
2021

13. Statin therapy is associated with lower prevalence of gut microbiota dysbiosis

Author

Vieira-Silva, Sara, Falony, Gwen, Belda, Eugeni, Nielsen, Trine, Aron-Wisnewsky, Judith, Chakaroun, Rima, Forslund, Sofia K, Assmann, Karen, Valles-Colomer, Mireia, Nguyen, Thi Thuy Duyen, Proost, Sebastian, Prifti, Edi, Tremaroli, Valentina, Pons, Nicolas, Le Chatelier, Emmanuelle, Andreelli, Fabrizio, Bastard, Jean-Phillippe, Coelho, Luis Pedro, Galleron, Nathalie, Hansen, Tue H, Hulot, Jean-Sébastien, Lewinter, Christian, Pedersen, Helle K, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Søndertoft, Nadja B, Touch, Sothea, Dumas, Marc-Emmanuel, Ehrlich, Stanislav Dusko, Galan, Pilar, Gøtze, Jens P, Hansen, Torben, Holst, Jens J, Køber, Lars, Letunic, Ivica, Nielsen, Jens, Oppert, Jean-Michel, Stumvoll, Michael, Vestergaard, Henrik, Zucker, Jean-Daniel, Bork, Peer, Pedersen, Oluf, Bäckhed, Fredrik, Clément, Karine, Raes, Jeroen, Vieira-Silva, Sara, Falony, Gwen, Belda, Eugeni, Nielsen, Trine, Aron-Wisnewsky, Judith, Chakaroun, Rima, Forslund, Sofia K, Assmann, Karen, Valles-Colomer, Mireia, Nguyen, Thi Thuy Duyen, Proost, Sebastian, Prifti, Edi, Tremaroli, Valentina, Pons, Nicolas, Le Chatelier, Emmanuelle, Andreelli, Fabrizio, Bastard, Jean-Phillippe, Coelho, Luis Pedro, Galleron, Nathalie, Hansen, Tue H, Hulot, Jean-Sébastien, Lewinter, Christian, Pedersen, Helle K, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Søndertoft, Nadja B, Touch, Sothea, Dumas, Marc-Emmanuel, Ehrlich, Stanislav Dusko, Galan, Pilar, Gøtze, Jens P, Hansen, Torben, Holst, Jens J, Køber, Lars, Letunic, Ivica, Nielsen, Jens, Oppert, Jean-Michel, Stumvoll, Michael, Vestergaard, Henrik, Zucker, Jean-Daniel, Bork, Peer, Pedersen, Oluf, Bäckhed, Fredrik, Clément, Karine, and Raes, Jeroen

Abstract

Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease2. Reported changes in stool consistency3 and inflammation status4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible

Published
2020

14. Statin therapy is associated with lower prevalence of gut microbiota dysbiosis

Author

Vieira-Silva, Sara, Falony, Gwen, Belda, Eugeni, Nielsen, Trine, Aron-Wisnewsky, Judith, Chakaroun, Rima, Forslund, Sofia K, Assmann, Karen, Valles-Colomer, Mireia, Nguyen, Thi Thuy Duyen, Proost, Sebastian, Prifti, Edi, Tremaroli, Valentina, Pons, Nicolas, Le Chatelier, Emmanuelle, Andreelli, Fabrizio, Bastard, Jean-Phillippe, Coelho, Luis Pedro, Galleron, Nathalie, Hansen, Tue H, Hulot, Jean-Sébastien, Lewinter, Christian, Pedersen, Helle K, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Søndertoft, Nadja B, Touch, Sothea, Dumas, Marc-Emmanuel, Ehrlich, Stanislav Dusko, Galan, Pilar, Gøtze, Jens P, Hansen, Torben, Holst, Jens J, Køber, Lars, Letunic, Ivica, Nielsen, Jens, Oppert, Jean-Michel, Stumvoll, Michael, Vestergaard, Henrik, Zucker, Jean-Daniel, Bork, Peer, Pedersen, Oluf, Bäckhed, Fredrik, Clément, Karine, Raes, Jeroen, Vieira-Silva, Sara, Falony, Gwen, Belda, Eugeni, Nielsen, Trine, Aron-Wisnewsky, Judith, Chakaroun, Rima, Forslund, Sofia K, Assmann, Karen, Valles-Colomer, Mireia, Nguyen, Thi Thuy Duyen, Proost, Sebastian, Prifti, Edi, Tremaroli, Valentina, Pons, Nicolas, Le Chatelier, Emmanuelle, Andreelli, Fabrizio, Bastard, Jean-Phillippe, Coelho, Luis Pedro, Galleron, Nathalie, Hansen, Tue H, Hulot, Jean-Sébastien, Lewinter, Christian, Pedersen, Helle K, Quinquis, Benoit, Rouault, Christine, Roume, Hugo, Salem, Joe-Elie, Søndertoft, Nadja B, Touch, Sothea, Dumas, Marc-Emmanuel, Ehrlich, Stanislav Dusko, Galan, Pilar, Gøtze, Jens P, Hansen, Torben, Holst, Jens J, Køber, Lars, Letunic, Ivica, Nielsen, Jens, Oppert, Jean-Michel, Stumvoll, Michael, Vestergaard, Henrik, Zucker, Jean-Daniel, Bork, Peer, Pedersen, Oluf, Bäckhed, Fredrik, Clément, Karine, and Raes, Jeroen

Abstract

Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease2. Reported changes in stool consistency3 and inflammation status4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible

Published
2020

15. Extending the cereus group genomics to putative food-borne pathogens of different toxicity

Author

Lapidus, Alla, Lapidus, Alla, Goltsman, Eugene, Auger, Sandrine, Galleron, Nathalie, Segurens, Beatrice, Dossat, Carole, Land, Miriam L., Broussole, Veronique, Brillard, Julien, Guinebretiere, Marie-Helene, Sanchis, Vincent, Nguen-the, Christophe, Lereclus, Didier, Richardson, Paul, Winker, Patrick, Weissenbach, Jean, Ehrlich, S.Dusko, Sorokin, Alexei, Lapidus, Alla, Lapidus, Alla, Goltsman, Eugene, Auger, Sandrine, Galleron, Nathalie, Segurens, Beatrice, Dossat, Carole, Land, Miriam L., Broussole, Veronique, Brillard, Julien, Guinebretiere, Marie-Helene, Sanchis, Vincent, Nguen-the, Christophe, Lereclus, Didier, Richardson, Paul, Winker, Patrick, Weissenbach, Jean, Ehrlich, S.Dusko, and Sorokin, Alexei

Abstract

The cereus group represents sporulating soil bacteria containing pathogenic strains which may cause diarrheic or emetic food poisoning outbreaks. Multiple locus sequence typing revealed a presence in natural samples of these bacteria of about thirty clonal complexes. Application of genomic methods to this group was however biased due to the major interest for representatives closely related to B. anthracis. Albeit the most important food-borne pathogens were not yet defined, existing data indicate that they are scattered all over the phylogenetic tree. The preliminary analysis of the sequences of three genomes discussed in this paper narrows down the gaps in our knowledge of the cereus group. The strain NVH391-98 is a rare but particularly severe food-borne pathogen. Sequencing revealed that the strain must be a representative of a novel bacterial species, for which the name Bacillus cytotoxis is proposed. This strain has a reduced genome size compared to other cereus group strains. Genome analysis revealed absence of sigma B factor and the presence of genes encoding diarrheic Nhe toxin, not detected earlier. The strain B. cereus F837/76 represents a clonal complex close to that of B. anthracis. Including F837/76, three such B. cereus strains had been sequenced. Alignment of genomes suggests that B. anthracis is their common ancestor. Since such strains often emerge from clinical cases, they merit a special attention. The third strain, KBAB4, is a typical psychrotrophe characteristic to unbiased soil communities. Phylogenic studies show that in nature it is the most active group in terms of gene exchange. Genomic sequence revealed high presence of extra-chromosomal genetic material (about 530 kb) that may account for this phenomenon. Genes coding Nhe-like toxin were found on a big plasmid in this strain. This may indicate a potential mechanism of toxicity spread from the psychrotrophic strain community. The results of this genomic work and ecological compartments of

Published
2008

16. Extending the cereus group genomics to putative food-borne pathogens of different toxicity

Author

Lapidus, Alla, Lapidus, Alla, Goltsman, Eugene, Auger, Sandrine, Galleron, Nathalie, Segurens, Beatrice, Dossat, Carole, Land, Miriam L., Broussole, Veronique, Brillard, Julien, Guinebretiere, Marie-Helene, Sanchis, Vincent, Nguen-the, Christophe, Lereclus, Didier, Richardson, Paul, Winker, Patrick, Weissenbach, Jean, Ehrlich, S.Dusko, Sorokin, Alexei, Lapidus, Alla, Lapidus, Alla, Goltsman, Eugene, Auger, Sandrine, Galleron, Nathalie, Segurens, Beatrice, Dossat, Carole, Land, Miriam L., Broussole, Veronique, Brillard, Julien, Guinebretiere, Marie-Helene, Sanchis, Vincent, Nguen-the, Christophe, Lereclus, Didier, Richardson, Paul, Winker, Patrick, Weissenbach, Jean, Ehrlich, S.Dusko, and Sorokin, Alexei

Abstract

The cereus group represents sporulating soil bacteria containing pathogenic strains which may cause diarrheic or emetic food poisoning outbreaks. Multiple locus sequence typing revealed a presence in natural samples of these bacteria of about thirty clonal complexes. Application of genomic methods to this group was however biased due to the major interest for representatives closely related to B. anthracis. Albeit the most important food-borne pathogens were not yet defined, existing data indicate that they are scattered all over the phylogenetic tree. The preliminary analysis of the sequences of three genomes discussed in this paper narrows down the gaps in our knowledge of the cereus group. The strain NVH391-98 is a rare but particularly severe food-borne pathogen. Sequencing revealed that the strain must be a representative of a novel bacterial species, for which the name Bacillus cytotoxis is proposed. This strain has a reduced genome size compared to other cereus group strains. Genome analysis revealed absence of sigma B factor and the presence of genes encoding diarrheic Nhe toxin, not detected earlier. The strain B. cereus F837/76 represents a clonal complex close to that of B. anthracis. Including F837/76, three such B. cereus strains had been sequenced. Alignment of genomes suggests that B. anthracis is their common ancestor. Since such strains often emerge from clinical cases, they merit a special attention. The third strain, KBAB4, is a typical psychrotrophe characteristic to unbiased soil communities. Phylogenic studies show that in nature it is the most active group in terms of gene exchange. Genomic sequence revealed high presence of extra-chromosomal genetic material (about 530 kb) that may account for this phenomenon. Genes coding Nhe-like toxin were found on a big plasmid in this strain. This may indicate a potential mechanism of toxicity spread from the psychrotrophic strain community. The results of this genomic work and ecological compartments of

Published
2008

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