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• W2201469345 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 (<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>G</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>d</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>) and suboptimal (<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M2><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>S</mml:mi><mml:mi mathvariant=normal>u</mml:mi><mml:mi mathvariant=normal>b</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>p</mml:mi><mml:mi mathvariant=normal>t</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>) asthma symptom control. Methods . Peripheral blood neutrophils from<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M3><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>G</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>d</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>(ACQ < 0.75,<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M4><mml:mi>n</mml:mi><mml:mo>=</mml:mo><mml:mn>11</mml:mn></mml:math>),<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M5><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>S</mml:mi><mml:mi mathvariant=normal>u</mml:mi><mml:mi mathvariant=normal>b</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>p</mml:mi><mml:mi mathvariant=normal>t</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>(ACQ > 0.75,<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M6><mml:mi>n</mml:mi><mml:mo>=</mml:mo><mml:mn>7</mml:mn></mml:math>), and healthy controls (HC) (<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M7><mml:mi>n</mml:mi><mml:mo>=</mml:mo><mml:mn>9</mml:mn></mml:math>) 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<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M8><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>G</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>d</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>neutrophils compared to HC. fMLF stimulated neutrophils from<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M9><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>S</mml:mi><mml:mi mathvariant=normal>u</mml:mi><mml:mi mathvariant=normal>b</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>p</mml:mi><mml:mi mathvariant=normal>t</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>but not<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M10><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>G</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>d</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>produced 50% of HC levels. fMLF induced MMP-9 was impaired in<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M11><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>S</mml:mi><mml:mi mathvariant=normal>u</mml:mi><mml:mi mathvariant=normal>b</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>p</mml:mi><mml:mi mathvariant=normal>t</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>and<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M12><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>G</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>d</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>compared to HC. fMLF stimulated CXCL8 but not MMP-9 was positively correlated with FEV 1 and FEV 1 /FVC.<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M13><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>S</mml:mi><mml:mi mathvariant=normal>u</mml:mi><mml:mi mathvariant=normal>b</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>p</mml:mi><mml:mi mathvariant=normal>t</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>and<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M14><mml:mrow><mml:msub><mml:mrow><mml:mi mathvariant=normal>A</mml:mi></mml:mrow><mml:mrow><mml:mi mathvariant=normal>G</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>o</mml:mi><mml:mi mathvariant=normal>d</mml:mi></mml:mrow></mml:msub></mml:mrow></mml:math>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." @default.
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• W2201469345 date "2015-01-01" @default.
• W2201469345 modified "2023-10-17" @default.
• W2201469345 title "Altered Innate Immune Responses in Neutrophils from Patients with Well- and Suboptimally Controlled Asthma" @default.
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• W2201469345 doi "https://doi.org/10.1155/2015/219374" @default.
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