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sTREM‐1 is elevated in cystic fibrosis and correlates with proteases
Author(s) -
Forrester D.L.,
Barr H.L.,
Fogarty A.,
Knox A.
Publication year - 2017
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.23650
Subject(s) - medicine , proteases , cystic fibrosis , neutrophil elastase , exacerbation , elastase , biomarker , protease , immunology , gastroenterology , fibrosis , inflammation , enzyme , biology , biochemistry
Summary Background sTREM‐1 (soluble triggering receptor expressed on myeloid cells‐1) is a novel inflammatory marker that may be of clinical use in cystic fibrosis (CF). Dysregulation of the TREM pathway has been demonstrated in other inflammatory diseases and modulation in animal models has therapeutic benefit. We hypothesised that sTREM‐1 could act as a biomarker of disease in cystic fibrosis. Methods Plasma from 17 patients with CF (stable and pre and post pulmonary exacerbation) and eight healthy volunteers was analyzed for sTREM‐1 and proteases (matrix metalloproteinase‐8 (MMP‐8), MMP‐9, and human neutrophil elastase HNE). Results sTREM‐1 Levels were elevated in stable CF subjects compared to controls (148 pg/ml (130–160) [median(IQR)] vs. 87 (55–118) ( P < 0.01)) but were not further increased during pulmonary exacerbation nor decreased after antibiotic treatment in CF. Protease levels were increased in CF plasma compared to controls: MMP–8 = 3.1 ng/ml (1.5–7.6) vs. 0.3 (0.18–0.53) ( P < 0.01) (Wilcoxon); MMP–9 = 170 ng/ml (124–282) vs. 49 (39–90) ( P < 0.01); HNE = 30.2 ng/ml (22.7–30.9) vs. 17.5 (11.2–22.2) ( P < 0.05). sTREM‐1 correlated positively with protease levels lnMMP‐8 r 2 = 0.55 ( P = 0.08), lnMMP‐9 r 2 = 0.61( P < 0.05), lnHNE r 2 = 0.35 ( P < 0.05). Conclusions sTREM‐1 is constitutively elevated in CF and positively correlates with protease levels. Modulation of this pathway may be of therapeutic benefit to patients with CF. Pediatr Pulmonol. 2017;52:467–471. © 2017 Wiley Periodicals, Inc.