Tuberculosis causes highly conserved metabolic changes in human patients, mycobacteria-infected mice and zebrafish larvae
bioRxiv (Cold Spring Harbor Laboratory)
Abstract
Abstract Tuberculosis is a highly infectious and potentially fatal disease accompanied by wasting symptoms, which cause severe metabolic changes in infected people. In this study we have compared the effect of mycobacteria infection on the level of metabolites in blood of humans and mice and whole zebrafish larvae using one highly standardized mass spectrometry pipeline, ensuring technical comparability of the results. Quantification of a range of circulating small amines showed that the levels of the majority of these compounds were significantly decreased in all three groups of infected organisms. Ten of these metabolites were common between the three different organisms comprising: methionine, asparagine, cysteine, threonine, serine, tryptophan, leucine, citrulline, ethanolamine and phenylalanine. The metabolomic changes of zebrafish larvae after infection were confirmed by nuclear magnetic resonance spectroscopy. Our study identified common biomarkers for tuberculosis disease in humans, mice and zebrafish, showing across species conservation of metabolic reprogramming processes as a result of disease. Apparently, the mechanisms underlying these processes are independent of environmental, developmental and vertebrate evolutionary factors. The zebrafish larval model is highly suited to further investigate the mechanism of metabolic reprogramming and the connection with wasting syndrome due to infection by mycobacteria.
Authors 13
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Affiliation as printed
Institute of Biology, Leiden University, The Netherlands
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Affiliation as printed
Leiden Academic Centre for Drug Research, Leiden University, The Netherlands
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Leiden University · Max Planck Institute for Heart and Lung Research
Affiliation as printed
Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany
Institute of Biology, Leiden University, The Netherlands
Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, 1231 Bad Nauheim, Germany
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Affiliation as printed
Institute of Biology, Leiden University, The Netherlands
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Affiliation as printed
Leiden Academic Centre for Drug Research, Leiden University, The Netherlands
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Leiden University Medical Center
Affiliation as printed
Department of Infectious Diseases, Leiden University Medical Center, The Netherlands
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Leiden University Medical Center
Affiliation as printed
Department of Infectious Diseases, Leiden University Medical Center, The Netherlands
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Leiden University Medical Center
Affiliation as printed
Department of Infectious Diseases, Leiden University Medical Center, The Netherlands
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Leiden University Medical Center
Affiliation as printed
Department of Infectious Diseases, Leiden University Medical Center, The Netherlands
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Affiliation as printed
Leiden Academic Centre for Drug Research, Leiden University, The Netherlands
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A. Alia Aachen
Leiden University · Leipzig University
Affiliation as printed
Institute for Medical Physics and Biophysics, University of Leipzig, 04107 Leipzig, Germany
Leiden Institute of Chemistry, Leiden University, 2333 Leiden, The Netherlands
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Affiliation as printed
Leiden Academic Centre for Drug Research, Leiden University, The Netherlands
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Affiliation as printed
Institute of Biology, Leiden University, The Netherlands
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