title: Circulating galectin-3 in infections and non-infectious inflammatory diseases.
abstract: Recent studies point to a dual role for galectin-3 as both a circulating damage-associated molecular pattern and a cell membrane-associated pattern recognition receptor. The aim of this study was to assess the potential of circulating galectin-3 for discriminating between infections and non-infectious inflammatory disorders on the one hand, and between fungal and bacterial infections on the other. Galectin-3 and C-reactive protein (CRP) were measured in the plasma of 127 patients with either non-infectious inflammatory disorders (gout, autoinflammatory syndrome or pancreatitis) or an infection (viral lower respiratory tract infection, bacterial sepsis or candidaemia). Circulating galectin-3 concentrations were increased in patients with infections when compared with healthy volunteers or patients with non-infectious inflammatory diseases. At cut-off values with a specificity of 95%, the sensitivity of galectin-3 (>20.6 ng/ml) to discriminate between an infection and non-infectious inflammation was higher than that of CRP (>156 mg/l): 43% [95% confidence interval (CI) 33-53%] versus 27% (95% CI 19-37%), p = 0.03. After exclusion of patients with CRP <156 mg/l, galectin-3 concentration >20.6 ng/ml could identify 41 % (95% CI 29-53%) of the patients with an infection at the cost of one false-positive with non-infectious inflammation. Using this sequential approach, 57% of the patients with an infection could be selected. Galectin-3 concentrations were similar in patients with bacterial and Candida sepsis, while being lower in viral respiratory infections. Although galectin-3 does not discriminate between bacterial and Candida sepsis, the sequential use of CRP and galectin-3 in distinguishing infectious diseases from non-infectious inflammation may be superior to CRP alone.
authors.affiliation: Department of Medicine, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands, j.tenoever@aig.umcn.nl.
authors.forename: J
authors.initials: J
authors.lastname: ten Oever
authors.forename: E J
authors.initials: EJ
authors.lastname: Giamarellos-Bourboulis
authors.forename: F L
authors.initials: FL
authors.lastname: van de Veerdonk
authors.forename: F F
authors.initials: FF
authors.lastname: Stelma
authors.forename: A
authors.initials: A
authors.lastname: Simon
authors.forename: M
authors.initials: M
authors.lastname: Janssen
authors.forename: M
authors.initials: M
authors.lastname: Johnson
authors.forename: A
authors.initials: A
authors.lastname: Pachot
authors.forename: B-J
authors.initials: BJ
authors.lastname: Kullberg
authors.forename: L A B
authors.initials: LA
authors.lastname: Joosten
authors.forename: M G
authors.initials: MG
authors.lastname: Netea
mesh_terms: D001327:Autoimmune Diseases / Q000097:blood; D016470:Bacteremia / Q000097:blood; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003141:Communicable Diseases / Q000097:blood*; D005260:Female; D037502:Galectin 3 / Q000097:blood*; D006073:Gout / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000097:blood
chemical_list: D015415:Biomarkers; D037502:Galectin 3; D002097:C-Reactive Protein