Volume 121, Issue 3 , Pages 685-691, March 2008
Increased sputum and bronchial biopsy IL-13 expression in severe asthma
Background
The importance of IL-13 in the asthma paradigm is supported by increased expression in human subjects, particularly in patients with mild-to-moderate asthma. However, the role of IL-13 in severe asthma needs to be further defined.
Objective
We sought to assess IL-13 expression in sputum and bronchial biopsy specimens from subjects with mild-to-severe asthma.
Methods
Sputum IL-13 concentrations were measured in 32 control subjects, 34 subjects with mild asthma, 21 subjects with moderate asthma, and 26 subjects with severe asthma. Enumeration of mast cells, eosinophils, and IL-13+ cells in the bronchial submucosa and airway smooth muscle (ASM) bundle was performed in 7 control subjects, 14 subjects with mild asthma, 7 subjects with moderate asthma, and 7 subjects with severe asthma.
Results
The proportion of subjects with measurable IL-13 in the sputum was increased in the mild asthma group (15/34) and severe asthma group (10/26) compared with that seen in the control group (4/32; P = .004). IL-13+ cells were increased within the submucosa in all asthma severity groups compared with control subjects (P = .006). The number of IL-13+ cells were increased within the ASM bundle in the severe asthma group compared with that seen in the other groups (P < .05). Asthma control questionnaire scores positively correlated with sputum IL-13 concentrations (Rs = 0.35, P = .04) and mast cells in the ASM bundle (Rs = 0.7, P = .007). IL-13+ cells within the submucosa and ASM correlated with sputum eosinophilia (Rs = 0.4, P ≤ .05).
Conclusions
IL-13 overexpression in sputum and bronchial biopsy specimens is a feature of severe asthma.
Key words: Severe asthma, IL-13, sputum, bronchus, airway smooth muscle, eosinophilia
Abbreviations used: ACQ, Juniper Asthma Control Questionnaire, AHR, Airway hyperresponsiveness, ASM, Airway smooth muscle, GINA, Global Initiative for Asthma
Supported by Asthma UK, Cambridge Antibody Technology, GlaxoSmithKline, and a DOH Clinical Scientist award.
Disclosure of potential conflict of interest: C. E. Brightling has consulting arrangements with AstraZeneca, GlaxoSmithKline, Cambridge Antibody Technology, and Roche; has received research support from AstraZeneca, Cambridge Antibody Technology, and GlaxoSmithKline; and is on the speakers' bureau for GlaxoSmithKline, AstraZeneca, and Pfizer. R. May is employed by and has equity in Cambridge Antibody Technology. P. Monk is employed by Synairgen Research Ltd. I. D. Pavord has received research support from GlaxoSmithKline and AstraZeneca. The rest of the authors have declared that they have no conflict of interest.
PII: S0091-6749(08)00126-7
doi:10.1016/j.jaci.2008.01.005
© 2008 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 121, Issue 3 , Pages 685-691, March 2008
