Gut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>

ABSTRACT The gut microbiota confers resistance to pathogens of the intestinal ecosystem, yet the dynamics of pathogen-microbiome interactions and the metabolites involved in this process remain largely unknown. Here, we use gnotobiotic mice infected with the virulent pathogen Salmonella enterica ser...

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Autores principales:	Jennifer R. Bratburd, Caitlin Keller, Eugenio Vivas, Erin Gemperline, Lingjun Li, Federico E. Rey, Cameron R. Currie
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2018
Materias:	Salmonella gut microbiome metabolomics metagenomics Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/31f43681d7254fa58155b130b3813ffd
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spelling	oai:doaj.org-article:31f43681d7254fa58155b130b3813ffd2021-11-15T15:52:19ZGut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>10.1128/mBio.02032-182150-7511https://doaj.org/article/31f43681d7254fa58155b130b3813ffd2018-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.02032-18https://doaj.org/toc/2150-7511ABSTRACT The gut microbiota confers resistance to pathogens of the intestinal ecosystem, yet the dynamics of pathogen-microbiome interactions and the metabolites involved in this process remain largely unknown. Here, we use gnotobiotic mice infected with the virulent pathogen Salmonella enterica serovar Typhimurium or the opportunistic pathogen Candida albicans in combination with metagenomics and discovery metabolomics to identify changes in the community and metabolome during infection. To isolate the role of the microbiota in response to pathogens, we compared mice monocolonized with the pathogen, uninfected mice “humanized” with a synthetic human microbiome, or infected humanized mice. In Salmonella-infected mice, by 3 days into infection, microbiome community structure and function changed substantially, with a rise in Enterobacteriaceae strains and a reduction in biosynthetic gene cluster potential. In contrast, Candida-infected mice had few microbiome changes. The LC-MS metabolomic fingerprint of the cecum differed between mice monocolonized with either pathogen and humanized infected mice. Specifically, we identified an increase in glutathione disulfide, glutathione cysteine disulfide, inosine 5’-monophosphate, and hydroxybutyrylcarnitine in mice infected with Salmonella in contrast to uninfected mice and mice monocolonized with Salmonella. These metabolites potentially play a role in pathogen-induced oxidative stress. These results provide insight into how the microbiota community members interact with each other and with pathogens on a metabolic level. IMPORTANCE The gut microbiota is increasingly recognized for playing a critical role in human health and disease, especially in conferring resistance to both virulent pathogens such as Salmonella, which infects 1.2 million people in the United States every year (E. Scallan, R. M. Hoekstra, F. J. Angulo, R. V. Tauxe, et al., Emerg Infect Dis 17:7–15, 2011, https://doi.org/10.3201/eid1701.P11101), and opportunistic pathogens like Candida, which causes an estimated 46,000 cases of invasive candidiasis each year in the United States (Centers for Disease Control and Prevention, Antibiotic Resistance Threats in the United States, 2013, 2013). Using a gnotobiotic mouse model, we investigate potential changes in gut microbial community structure and function during infection using metagenomics and metabolomics. We observe that changes in the community and in biosynthetic gene cluster potential occur within 3 days for the virulent Salmonella enterica serovar Typhimurium, but there are minimal changes with a poorly colonizing Candida albicans. In addition, the metabolome shifts depending on infection status, including changes in glutathione metabolites in response to Salmonella infection, potentially in response to host oxidative stress.Jennifer R. BratburdCaitlin KellerEugenio VivasErin GemperlineLingjun LiFederico E. ReyCameron R. CurrieAmerican Society for MicrobiologyarticleSalmonellagut microbiomemetabolomicsmetagenomicsMicrobiologyQR1-502ENmBio, Vol 9, Iss 6 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Salmonella gut microbiome metabolomics metagenomics Microbiology QR1-502
spellingShingle	Salmonella gut microbiome metabolomics metagenomics Microbiology QR1-502 Jennifer R. Bratburd Caitlin Keller Eugenio Vivas Erin Gemperline Lingjun Li Federico E. Rey Cameron R. Currie Gut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>
description	ABSTRACT The gut microbiota confers resistance to pathogens of the intestinal ecosystem, yet the dynamics of pathogen-microbiome interactions and the metabolites involved in this process remain largely unknown. Here, we use gnotobiotic mice infected with the virulent pathogen Salmonella enterica serovar Typhimurium or the opportunistic pathogen Candida albicans in combination with metagenomics and discovery metabolomics to identify changes in the community and metabolome during infection. To isolate the role of the microbiota in response to pathogens, we compared mice monocolonized with the pathogen, uninfected mice “humanized” with a synthetic human microbiome, or infected humanized mice. In Salmonella-infected mice, by 3 days into infection, microbiome community structure and function changed substantially, with a rise in Enterobacteriaceae strains and a reduction in biosynthetic gene cluster potential. In contrast, Candida-infected mice had few microbiome changes. The LC-MS metabolomic fingerprint of the cecum differed between mice monocolonized with either pathogen and humanized infected mice. Specifically, we identified an increase in glutathione disulfide, glutathione cysteine disulfide, inosine 5’-monophosphate, and hydroxybutyrylcarnitine in mice infected with Salmonella in contrast to uninfected mice and mice monocolonized with Salmonella. These metabolites potentially play a role in pathogen-induced oxidative stress. These results provide insight into how the microbiota community members interact with each other and with pathogens on a metabolic level. IMPORTANCE The gut microbiota is increasingly recognized for playing a critical role in human health and disease, especially in conferring resistance to both virulent pathogens such as Salmonella, which infects 1.2 million people in the United States every year (E. Scallan, R. M. Hoekstra, F. J. Angulo, R. V. Tauxe, et al., Emerg Infect Dis 17:7–15, 2011, https://doi.org/10.3201/eid1701.P11101), and opportunistic pathogens like Candida, which causes an estimated 46,000 cases of invasive candidiasis each year in the United States (Centers for Disease Control and Prevention, Antibiotic Resistance Threats in the United States, 2013, 2013). Using a gnotobiotic mouse model, we investigate potential changes in gut microbial community structure and function during infection using metagenomics and metabolomics. We observe that changes in the community and in biosynthetic gene cluster potential occur within 3 days for the virulent Salmonella enterica serovar Typhimurium, but there are minimal changes with a poorly colonizing Candida albicans. In addition, the metabolome shifts depending on infection status, including changes in glutathione metabolites in response to Salmonella infection, potentially in response to host oxidative stress.
format	article
author	Jennifer R. Bratburd Caitlin Keller Eugenio Vivas Erin Gemperline Lingjun Li Federico E. Rey Cameron R. Currie
author_facet	Jennifer R. Bratburd Caitlin Keller Eugenio Vivas Erin Gemperline Lingjun Li Federico E. Rey Cameron R. Currie
author_sort	Jennifer R. Bratburd
title	Gut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>
title_short	Gut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>
title_full	Gut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>
title_fullStr	Gut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>
title_full_unstemmed	Gut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>
title_sort	gut microbial and metabolic responses to <named-content content-type="genus-species">salmonella enterica</named-content> serovar typhimurium and <named-content content-type="genus-species">candida albicans</named-content>
publisher	American Society for Microbiology
publishDate	2018
url	https://doaj.org/article/31f43681d7254fa58155b130b3813ffd
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Gut Microbial and Metabolic Responses to <named-content content-type="genus-species">Salmonella enterica</named-content> Serovar Typhimurium and <named-content content-type="genus-species">Candida albicans</named-content>

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