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Anti-inflammatory deficiencies in neutrophilic asthma: reduced galectin-3 and IL-1RA/IL-1β.

Authors :
Peng Gao
Gibson, Peter G.
Baines, Katherine J.
Yang, Ian A.
Upham, John W.
Reynolds, Paul N.
Hodge, Sandra
James, Alan L.
Jenkins, Christine
Peters, Matthew J.
Jie Zhang
Simpson, Jodie L.
Source :
Respiratory Research; 2015, Vol. 16 Issue 1, p1-10, 10p, 6 Charts, 1 Graph
Publication Year :
2015

Abstract

Background: Galectin-3 (gal-3), a member of the β-galactoside-binding animal lectins, is involved in the recruitment, activation and removal of neutrophils. Neutrophilic asthma is characterized by a persistent elevation of airway neutrophils and impaired efferocytosis. We hypothesized that sputum gal-3 would be reduced in neutrophilic asthma and the expression of gal-3 would be associated with other markers of neutrophilic inflammation. Methods: Adults with asthma (n = 80) underwent a sputum induction following clinical assessment and blood collection. Sputum was dispersed for a differential cell count and ELISA assessment of gal-3, gal-3 binding protein (BP), interleukin (IL)-1β, IL-1 receptor antagonist (RA), IL-8 and IL-6. Gal-3 and gal-3BP immunoreactivity were assessed in mixed sputum cells. Results: Sputum gal-3 (median, (q1,q3)) was significantly reduced in neutrophilic asthma (183 ng/mL (91,287)) compared with eosinophilic (293 ng/mL (188,471), p = 0.021) and paucigranulocytic asthma (399 ng/mL (213,514), p = 0.004). The gal-3/gal-3BP ratio and IL-1RA/IL-1β ratio were significantly reduced, while gal-3BP and IL-1β were significantly elevated in neutrophilic asthma compared with eosinophilic and paucigranulocytic asthma. Conclusion: Patients with neutrophilic asthma have impairment in anti-inflammatory ratio of gal-3/gal-3BP and IL-1RA/IL-1β which provides a further framework for exploration into pathologic mechanisms of asthma phenotypes. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
14659921
Volume :
16
Issue :
1
Database :
Complementary Index
Journal :
Respiratory Research
Publication Type :
Academic Journal
Accession number :
101777655
Full Text :
https://doi.org/10.1186/s12931-014-0163-5