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Cited by 586COVID-19 Clinical Research StudiesTryptophan and brain disordersMetabolomics and Mass Spectrometry Studies

COVID-19 infection alters kynurenine and fatty acid metabolism, correlating with IL-6 levels and renal status

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Thomas, Tiffany, Stefanoni, Davide, Reisz, Julie A., Nemkov, Travis, Bertolone, Lorenzo, Francis, Richard O., Hudson, Krystalyn E., Zimring, James C. +4 more·2020·JCI Insight
DOI 10.1172/jci.insight.140327PMC PMC7453907

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Abstract

Previous studies suggest a role for systemic reprogramming of host metabolism during viral pathogenesis to fuel rapidly expanding viral proliferation, for example by providing free amino acids and fatty acids as building blocks. In addition, general alterations in metabolism can provide key understanding of pathogenesis. However, little is known about the specific metabolic effects of SARS-COV-2 infection. The present study evaluated the serum metabolism of COVID-19 patients (n=33), identified by a positive nucleic acid test of a nasopharyngeal swab, as compared to COVID-19-negative control patients (n=16). Targeted and untargeted metabolomics analyses specifically identified alterations in the metabolism of tryptophan into the kynurenine pathway, which is well-known to be involved in regulating inflammation and immunity. Indeed, the observed changes in tryptophan metabolism correlated with serum interleukin-6 (IL-6) levels. Metabolomics analysis also confirmed widespread dysregulation of nitrogen metabolism in infected patients, with decreased circulating levels of most amino acids, except for tryptophan metabolites in the kynurenine pathway, and increased markers of oxidant stress (e.g., methionine sulfoxide, cystine), proteolysis, and kidney dysfunction (e.g., creatine, creatinine, polyamines). Increased circulating levels of glucose and free fatty acids were also observed, consistent with altered carbon homeostasis in COVID-19 patients. Metabolite levels in these pathways correlated with clinical laboratory markers of inflammation and disease severity (i.e., IL-6 and C-reactive protein) and renal function (i.e., blood urea nitrogen). In conclusion, this initial observational study of the metabolic consequences of COVID-19 infection in a clinical cohort identified amino acid metabolism (especially kynurenine and cysteine/taurine) and fatty acid metabolism as correlates of COVID-19, providing mechanistic insights, potential markers of clinical severity, and potential therapeutic targets.

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  • Taurine has been linked to protection from inflammation in SARS-CoV-2 viral infection and reduces oxidative damage by formation of taurine haloamines.

    “In addition, taurine has been linked to protection from inflammation in SARS-CoV-2 viral infection and reduces oxidative damage by the formation of taurine haloamines.71,72”

    From Taurine lowers inflammaging by regulating the NLRP3 inflammasome in macrophages (2026) · cites this paper as [71]

    The Discussion (pp. 12–13) describes taurine as an antioxidant depleted in patients with COVID-19 and proposes taurine supplementation as a potential intervention. It does not show that taurine protects against inflammation during SARS-CoV-2 infection or say that it reduces oxidative damage through formation of taurine haloamines. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • KP activation during viral infections such as VEEV may drive the pathological interplay of inflammation and KYN dysregulation in the development or exacerbation of neurodegeneration.

    “This indicates KP activation during viral infections such as VEEV may drive the pathological interplay of inflammation and KYN dysregulation in the development or exacerbation of neurodegeneration [28,29,30].”

    From VEEV TC-83 Triggers Dysregulation of the Tryptophan–Kynurenine Pathway in the Central Nervous System That Correlates with Cognitive Impairment in Tg2576 Mice (2024) · cites this paper as [29]

    The Results (p. 1) report altered kynurenine-pathway metabolism in patients with COVID-19 and a correlation with IL-6; the Discussion (p. 8) says a role for IDO in inflammation is hypothetical and that causation cannot be inferred. The paper does not address VEEV or whether this interplay causes or worsens neurodegeneration. (LLM, conf=0.86)

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Authors
Thomas, T., Stefanoni, D., Reisz, J. A., Nemkov, T., Bertolone, L., Francis, R. O., Hudson, K. E., Zimring, J. C., Hansen, K. C., Hod, E. A., Spitalnik, S. L., & D’Alessandro, A.
Affiliations
  • Columbia University (US)
  • University of Colorado Anschutz (US)
  • University of Virginia (US)
Corresponding author
Spitalnik, Steven L.
ORCID
Venue
JCI Insight
Publisher
American Society for Clinical Investigation
Published
2020-07-23
Volume
5
Issue
14
ISSN
2379-3708 (ISSN-L)
DOI
10.1172/jci.insight.140327
PMC
PMC7453907
OpenAlex
W3036255694
Cited by
586
References
4
Citations by year
2026: 35 · 2025: 52 · 2024: 71 · 2023: 106 · 2022: 140 · 2021: 146 · 2020: 35
FWCI
13.93
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • JCI Insight (publishedVersion, cc-by)
  • medRxiv (acceptedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (submittedVersion)
Funders
  • Boettcher Webb-Waring Investigator Award (N/A)
  • National Heart, Lung, and Blood Institute (R01HL146442, R01HL149714, R01HL148151, R21HL150032, T32HL007171)
  • National Institute of General Medical Sciences (RM1GM131968)
Topics
  • Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolomics and Mass Spectrometry Studies
Keywords
COVID-19 pandemic, SARS-CoV-2, kynurenine pathway, tryptophan metabolism, fatty acid metabolism, interleukin-6, inflammation, renal dysfunction, amino acid metabolism, nitrogen metabolism, oxidative stress, serum metabolites, C-reactive protein, blood urea nitrogen

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