- Title
- Altered innate immune responses in neutrophils from patients with well- and suboptimally controlled asthma
- Creator
- Tang, Francesca S. M.; Foxley, Gloria J.; Gibson, Peter G.; Burgess, Janette K.; Baines, Katherine J.; Oliver, Brian G.
- Relation
- Mediators of Inflammation Vol. 2015, p. 1-11
- Publisher Link
- http://dx.doi.org/10.1155/2015/219374
- Publisher
- Hindawi
- Resource Type
- journal article
- Date
- 2015
- Description
- 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 (AGood) and suboptimal (ASubopt) asthma symptom control. Methods: Peripheral blood neutrophils from AGood (ACQ < 0.75, n=11), ASubopt (ACQ > 0.75, n=7), and healthy controls (HC) (n=9) were stimulated with bacterial (LPS (1 g/mL), fMLF (100 nM)), and viral (imiquimod (3 g/mL), R848 (1.5 g/mL), and poly I:C (10 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 AGood neutrophils compared to HC. fMLF stimulated neutrophils from ASubopt but not AGood produced 50% of HC levels. fMLF induced MMP-9 was impaired in ASubopt and AGood compared to HC. fMLF stimulated CXCL8 but not MMP-9 was positively correlated with FEV1 and FEV1/FVC. ASubopt and AGood 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.
- Subject
- asthma management; respiratory infections; neutrophilic inflammation
- Identifier
- http://hdl.handle.net/1959.13/1313381
- Identifier
- uon:22587
- Identifier
- ISSN:0962-9351
- Language
- eng
- Full Text
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