In:
Mediators of Inflammation, Hindawi Limited, Vol. 2015 ( 2015), p. 1-11
Abstract:
Background . Respiratory infections are a major cause of asthma exacerbations where neutrophilic inflammation dominates and is associated with steroid refractory asthma. Structural airway cells in asthma differ from nonasthmatics; however it is unknown if neutrophils differ. We investigated neutrophil immune responses in patients who have good ( A G o o d ) and suboptimal ( A S u b o p t ) asthma symptom control. Methods . Peripheral blood neutrophils from A G o o d (ACQ 〈 0.75, n = 11 ), A S u b o p t (ACQ 〉 0.75, n = 7 ), and healthy controls (HC) ( n = 9 ) were stimulated with bacterial (LPS (1 μ g/mL), fMLF (100 nM)), and viral (imiquimod (3 μ g/mL), R848 (1.5 μ g/mL), and poly I:C (10 μ g/mL)) surrogates or live rhinovirus (RV) 16 (MOI1). Cell-free supernatant was collected after 1 h for neutrophil elastase (NE) and matrix metalloproteinase- (MMP-) 9 measurements or after 24 h for CXCL8 release. Results . Constitutive NE was enhanced in A G o o d neutrophils compared to HC. fMLF stimulated neutrophils from A S u b o p t but not A G o o d produced 50% of HC levels. fMLF induced MMP-9 was impaired in A S u b o p t and A G o o d compared to HC. fMLF stimulated CXCL8 but not MMP-9 was positively correlated with FEV 1 and FEV 1 /FVC. A S u b o p t and A G o o d responded similarly to other stimuli. Conclusions . Circulating neutrophils are different in asthma; however, this is likely to be related to airflow limitation rather than asthma control.
Type of Medium:
Online Resource
ISSN:
0962-9351
,
1466-1861
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2015
detail.hit.zdb_id:
2008065-7
Permalink