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Original Research |

The Neutrophilic Inflammatory Phenotype Is Associated With Systemic Inflammation in AsthmaSystemic Inflammation in Neutrophilic Asthma

Lisa G. Wood, PhD; Katherine J. Baines, PhD; Juanjuan Fu, MD; Hayley A. Scott, BND; Peter G. Gibson, MBBS
Author and Funding Information

From the Centre for Asthma and Respiratory Diseases, University of Newcastle, and Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, Newcastle, NSW, Australia.

Correspondence to: Lisa G. Wood, PhD, Department Respiratory and Sleep Medicine, Level 3, Hunter Medical Research Institute, John Hunter Hospital, Locked Bag 1, Hunter Region Mail Centre, NSW, 2310, Australia; e-mail: lisa.wood@newcastle.edu.au

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Gibson is the recipient of a National Health and Medical Research Council of Australia Practitioner Fellowship. The remaining authors report no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Funding/Support: The authors have reported to CHEST that no funding was received for this study.


Funding/Support: The authors have reported to CHEST that no funding was received for this study.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2012;142(1):86-93. doi:10.1378/chest.11-1838
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Background:  The role of systemic inflammation in asthma is unclear. The aim of this study was to compare systemic inflammation in subjects with stable asthma, categorized by airway inflammatory phenotype, with healthy control subjects.

Methods:  Adults with stable asthma (n = 152) and healthy control subjects (n = 83) underwent hypertonic saline challenge and sputum induction. Differential leukocyte counts were performed on selected sputum. Plasma high-sensitivity C-reactive protein (CRP), IL-6, and tumor necrosis factor-α levels and sputum IL-8 and neutrophil elastase levels were determined by enzyme-linked immunosorbent assay. Sputum IL-8 receptor α (IL-8RA) and IL-8 receptor β (IL-8RB) messenger RNA expression were determined by real-time polymerase chain reaction.

Results:  Subjects with asthma were classified as having nonneutrophilic asthma or neutrophilic asthma. The asthma (neutrophilic) group had increased systemic inflammation compared with the asthma (nonneutrophilic) and healthy control groups, with median (interquartile range) CRP levels of 5.0 (1.6-9.2), 1.8 (0.9-5.3), and 1.8 (0.8-4.1) mg/L (P = .011), respectively, and IL-6 levels of 2.1 (1.5-3.1), 1.4 (1.0-2.1), and 1.1 (0.8-1.5) pg/mL (P < .001), respectively. The proportion of subjects with elevated CRP and IL-6 levels was also higher in the asthma (neutrophilic) group. Sputum IL-8 and neutrophil elastase protein and IL-8RA and IL-8RB gene expression were significantly increased in the asthma (neutrophilic) group. In multiple regression analysis of subjects with asthma, sex, BMI, statin use, and percent sputum neutrophils were significant predictors of log10CRP. Sex, BMI, and %FEV1 were significant predictors of log10IL-6.

Conclusions:  Systemic inflammation is increased in patients with asthma with neutrophilic airway inflammation and associated with worse clinical outcomes. Systemic inflammation may contribute to the pathophysiology of neutrophilic asthma.

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