TABLE 1

Proteins and metabolites defining progression from LTBI to active TB disease, response to antituberculosis treatment and treatment outcome

Clinical questionProteinsMetabolitesMaterial
LTBI to active TB transitionChemokines CCL1, CCL3, CXCL1, CXCL2, CXCL9, CXCL10 [73], kallikrein 1B, C-reactive protein, haptoglobin, alpha-1-acid glycoprotein 1 haptoglobin, complement component C9, apolipoprotein A1, serotransferrin [74]Cortisol, mannose, gamma-glutamylglutamine, cysteine, glycocholenate sulfate, phenylalanine, histidine, citrulline, glutamine, tryptophan [75]Blood
Treatment responseChemokines CCL1, CCL3, CXCL1, CXCL9 [73], nectin-life protein 2, Ephrin type-A receptor 1, gp130, beta-Ala-His dipeptidase, transforming growth factor-beta receptor III, mannose receptor C type 2, disintegrin and metalloproteinase domain-containing protein 9, cell adhesion molecule-related/downregulated by oncogenes [76]Blood
Matrix metalloproteinases MMP-2, MMP-3, MMP-8, MMP-9, tissue inhibitors of metalloproteinases TIMP-1 and TIMP-2 [77]Sputum
Seryl-leucine core 1 O-glycosylated peptide [78]Urine
Treatment outcomeChemokines CCL1, CCL2, CXCL2, CXCL9, CXCL10, CXCL11 [73]Blood
Matrix metalloproteinases MMP-1, MMP-3, MMP-8, tissue inhibitor of metalloproteinases TIMP-2 [77]Sputum
Tryptophan [79]CSF (TB meningitis)

LTBI: latent tuberculosis infection; TB: tuberculosis; CSF: cerebrospinal fluid.