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Increased Urinary Trimethylamine N -Oxide Following Cryptosporidium Infection and Protein Malnutrition Independent of Microbiome Effects

We have reported altered choline and tryptophan metabolism with malnutrition in our murine model and in children. Here, we report the additional metabolitic alterations with murine cryptosporidiosis, including trimethylamine N -oxide (TMAO), which is largely independent of changes in microbiota. Cry... Full description

Journal Title: The Journal of Infectious Diseases 2017, Vol. 216(1), pp.64-71
Main Author: Bolick, David T
Other Authors: Mayneris - Perxachs, Jordi , Medlock, Greg L , Kolling, Glynis L , Papin, Jason A , Swann, Jon R , Guerrant, Richard L
Format: Electronic Article Electronic Article
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ID: ISSN: 0022-1899 ; E-ISSN: 1537-6613 ; DOI: 10.1093/infdis/jix234
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recordid: oxford10.1093/infdis/jix234
title: Increased Urinary Trimethylamine N -Oxide Following Cryptosporidium Infection and Protein Malnutrition Independent of Microbiome Effects
format: Article
creator:
  • Bolick, David T
  • Mayneris - Perxachs, Jordi
  • Medlock, Greg L
  • Kolling, Glynis L
  • Papin, Jason A
  • Swann, Jon R
  • Guerrant, Richard L
subjects:
  • Choline
  • Cryptosporidium
  • Malnutrition
  • Metabonome
  • Microbiome
  • .
ispartof: The Journal of Infectious Diseases, 2017, Vol. 216(1), pp.64-71
description: We have reported altered choline and tryptophan metabolism with malnutrition in our murine model and in children. Here, we report the additional metabolitic alterations with murine cryptosporidiosis, including trimethylamine N -oxide (TMAO), which is largely independent of changes in microbiota. Cryptosporidium infections have been associated with growth stunting, even in the absence of diarrhea. Having previously detailed the effects of protein deficiency on both microbiome and metabolome in this model, we now describe the specific gut microbial and biochemical effects of Cryptosporidium infection. Protein-deficient mice were infected with Cryptosporidium parvum oocysts for 6–13 days and compared with uninfected controls. Following infection, there was an increase in the urinary excretion of choline- and amino-acid-derived metabolites. Conversely, infection reduced the excretion of the microbial–host cometabolite (3-hydroxyphenyl)propionate-sulfate and disrupted metabolites involved in the tricarboxylic acid (TCA) cycle. Correlation analysis of microbial and biochemical profiles resulted in associations between various microbiota members and TCA cycle metabolites, as well as some microbial-specific degradation products. However, no correlation was observed between the majority of the infection-associated metabolites and the fecal bacteria, suggesting that these biochemical perturbations are independent of concurrent changes in the relative abundance of members of the microbiota. We conclude that cryptosporidial infection in protein-deficient mice can mimic some metabolic changes seen in malnourished children and may help elucidate our understanding of long-term metabolic consequences of early childhood enteric infections.
language:
source:
identifier: ISSN: 0022-1899 ; E-ISSN: 1537-6613 ; DOI: 10.1093/infdis/jix234
fulltext: fulltext
issn:
  • 0022-1899
  • 00221899
  • 1537-6613
  • 15376613
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titleIncreased Urinary Trimethylamine N -Oxide Following Cryptosporidium Infection and Protein Malnutrition Independent of Microbiome Effects
creatorBolick, David T ; Mayneris - Perxachs, Jordi ; Medlock, Greg L ; Kolling, Glynis L ; Papin, Jason A ; Swann, Jon R ; Guerrant, Richard L
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subjectCholine ; Cryptosporidium ; Malnutrition ; Metabonome ; Microbiome ; .
descriptionWe have reported altered choline and tryptophan metabolism with malnutrition in our murine model and in children. Here, we report the additional metabolitic alterations with murine cryptosporidiosis, including trimethylamine N -oxide (TMAO), which is largely independent of changes in microbiota. Cryptosporidium infections have been associated with growth stunting, even in the absence of diarrhea. Having previously detailed the effects of protein deficiency on both microbiome and metabolome in this model, we now describe the specific gut microbial and biochemical effects of Cryptosporidium infection. Protein-deficient mice were infected with Cryptosporidium parvum oocysts for 6–13 days and compared with uninfected controls. Following infection, there was an increase in the urinary excretion of choline- and amino-acid-derived metabolites. Conversely, infection reduced the excretion of the microbial–host cometabolite (3-hydroxyphenyl)propionate-sulfate and disrupted metabolites involved in the tricarboxylic acid (TCA) cycle. Correlation analysis of microbial and biochemical profiles resulted in associations between various microbiota members and TCA cycle metabolites, as well as some microbial-specific degradation products. However, no correlation was observed between the majority of the infection-associated metabolites and the fecal bacteria, suggesting that these biochemical perturbations are independent of concurrent changes in the relative abundance of members of the microbiota. We conclude that cryptosporidial infection in protein-deficient mice can mimic some metabolic changes seen in malnourished children and may help elucidate our understanding of long-term metabolic consequences of early childhood enteric infections.
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titleIncreased Urinary Trimethylamine N -Oxide Following Cryptosporidium Infection and Protein Malnutrition Independent of Microbiome Effects
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abstractWe have reported altered choline and tryptophan metabolism with malnutrition in our murine model and in children. Here, we report the additional metabolitic alterations with murine cryptosporidiosis, including trimethylamine N -oxide (TMAO), which is largely independent of changes in microbiota. Cryptosporidium infections have been associated with growth stunting, even in the absence of diarrhea. Having previously detailed the effects of protein deficiency on both microbiome and metabolome in this model, we now describe the specific gut microbial and biochemical effects of Cryptosporidium infection. Protein-deficient mice were infected with Cryptosporidium parvum oocysts for 6–13 days and compared with uninfected controls. Following infection, there was an increase in the urinary excretion of choline- and amino-acid-derived metabolites. Conversely, infection reduced the excretion of the microbial–host cometabolite (3-hydroxyphenyl)propionate-sulfate and disrupted metabolites involved in the tricarboxylic acid (TCA) cycle. Correlation analysis of microbial and biochemical profiles resulted in associations between various microbiota members and TCA cycle metabolites, as well as some microbial-specific degradation products. However, no correlation was observed between the majority of the infection-associated metabolites and the fecal bacteria, suggesting that these biochemical perturbations are independent of concurrent changes in the relative abundance of members of the microbiota. We conclude that cryptosporidial infection in protein-deficient mice can mimic some metabolic changes seen in malnourished children and may help elucidate our understanding of long-term metabolic consequences of early childhood enteric infections.
pubOxford University Press
doi10.1093/infdis/jix234
date2017-07-01