Reprogramming of Amino Acid Metabolism Differs between Community-Acquired Pneumonia and Infection-Associated Exacerbation of Chronic Obstructive Pulmonary Disease

Cells. 2022 Jul 24;11(15):2283. doi: 10.3390/cells11152283.

Abstract

Amino acids and their metabolites are key regulators of immune responses, and plasma levels may change profoundly during acute disease states. Using targeted metabolomics, we evaluated concentration changes in plasma amino acids and related metabolites in community-acquired pneumonia (CAP, n = 29; compared against healthy controls, n = 33) from presentation to hospital through convalescence. We further aimed to identify biomarkers for acute CAP vs. the clinically potentially similar infection-triggered COPD exacerbation (n = 13). Amino acid metabolism was globally dysregulated in both CAP and COPD. Levels of most amino acids were markedly depressed in acute CAP, and total amino acid concentrations on admission were an accurate biomarker for the differentiation from COPD (AUC = 0.93), as were reduced asparagine and threonine levels (both AUC = 0.92). Reduced tryptophan and histidine levels constituted the most accurate biomarkers for acute CAP vs. controls (AUC = 0.96, 0.94). Only kynurenine, symmetric dimethyl arginine, and phenylalanine levels were increased in acute CAP, and the kynurenine/tryptophan ratio correlated best with clinical recovery and resolution of inflammation. Several amino acids did not reach normal levels by the 6-week follow-up. Glutamate levels were reduced on admission but rose during convalescence to 1.7-fold above levels measured in healthy control. Our data suggest that dysregulated amino acid metabolism in CAP partially persists through clinical recovery and that amino acid metabolism constitutes a source of promising biomarkers for CAP. In particular, total amino acids, asparagine, and threonine may constitute plasma biomarker candidates for the differentiation between CAP and infection-triggered COPD exacerbation and, perhaps, the detection of pneumonia in COPD.

Keywords: Staphylococcus aureus; amino acids; biogenic amines; biomarkers; chronic obstructive pulmonary disease; diagnosis; inflammation; metabolism; pathogenesis; pneumonia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asparagine
  • Biomarkers
  • Community-Acquired Infections* / diagnosis
  • Convalescence
  • Humans
  • Kynurenine
  • Pneumonia*
  • Pulmonary Disease, Chronic Obstructive*
  • Threonine
  • Tryptophan

Substances

  • Biomarkers
  • Threonine
  • Kynurenine
  • Asparagine
  • Tryptophan

Grants and funding

This study received support from the Innovative Medicines Initiative Joint Undertaking under Grant Agreement No. 115523-2–COMBACTE, resources of which are composed of financial contribution from the European Union’s Seventh Framework Programme (FP7/2007–2013) and EFPIA companies’ in kind contribution. It was also supported by iMed, the Helmholtz Association’s Cross Programme Initiative on Personalised Medicine (to F.P.) and by Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) Project-ID 97850925 (to A.S. and M.M.-H.). Haroon Arshad and Aamna Habib gratefully acknowledge support by Ph.D. student scholarships from the German Academic Exchange Service (DAAD)/Higher Education Commission of Pakistan. The funding bodies had no role in study design, in the collection, analysis, and interpretation of data, in the writing of the report, and in the decision to submit the paper for publication.