RESEARCH PAPER
IgE-dependent sensitization in patients with COPD
Andrzej Bożek 1  
,  
 
 
More details
Hide details
1
Clinical Department of Internal Disease, Dermatology and Allergology, Medical University of Silesia, Katowice, Poland
2
Clinical Department of Internal Diseases, Allergology and Clinical Immunology, Medical University of Silesia, Katowice, Poland
 
KEYWORDS:
TOPICS:
ABSTRACT:
Introduction and objective:
The aim of the study was to evaluate the differences between asthma and COPD on the basis of the prevalence and profile of IgE-dependent sensitization to inhaled allergens, and the blood serum levels of select Th1/Th2 cytokines.

Material and methods:
103 patients with COPD (114 patients with asthma and 121 controls) were included in the study. A skin prick test with common inhaled allergens was performed, and serum levels of IgE were measured in all subjects. Lymphocyte profiles were measured via the whole-blood method using fresh 10-ml blood samples treated with EDTA. The following surface antigens were measured: CD3, CD29, CD16, CD56, CD4, CD8, and HLA-DR. The Th1/Th2 profile in blood serum was determined using Th1/Th2 cytokine kits.

Results:
IgE-dependent sensitization to environmental allergens was found in 34 (33.3%) patients with COPD, 46 (40%) patients with asthma and in 14 (11.5%) volunteers. The odds ratio of sensitization in patients with COPD reached 0.89 (95% CI: 0.57–1.08) and it was more frequent than in the control population with an odds ratio of 0.71 (95% CI: 0.64–0.88). The serum concentration of IL-2 was significantly higher in patients with COPD and asthma than in controls. In the subgroup of patients with non-allergic asthma, similar serum concentrations were observed for all analyzed cytokines, except for IFN-gamma, which was lower in patients with COPD.

Conclusions:
Both the prevalence and profile of IgE-dependent sensitization to inhaled allergens did not differ between asthma and COPD. Both Th2 and Th1 played a role in the immunopathology of asthma and COPD.

Abbreviations:
COPD – Chronic Obstructive Pulmonary Disease; FEV1 – forced expiratory volume in one second; FVC – forced expiratory volume; GINA – Global Initiative for Asthma; GOLD – Global Initiative for Chronic Obstructive Lung Disease; MMRC – Modified Medical Research Council; Th1 – lymphocyte helper 1; Th2 – lymphocyte helper 2

CORRESPONDING AUTHOR:
Andrzej Bożek   
Clinical Department of Internal Disease, Dermatology and Allergology, Medical University of Silesia, Katowice, Skłodowskiej 10, 41-800 Zabrze, Poland
 
REFERENCES (22):
1. Barnes PJ. Therapeutic approaches to asthma-chronic obstructive pulmonary disease overlap syndromes. J Allergy Clin Immunol. 2015; 136: 531–45.
2. Global Initiative for Chronic Obstructive Lung Disease (GOLD) Updated 2015. http//: www.goldcopd.it/materiale/2015... (accessed 20.01.16).
3. Global Initiative for Asthma GINA. http//: www.gina.org/2015 (accessed 22.03.15).
4. Mathur SK, Viswanathan RK. Relevance of allergy in adult asthma. Curr Allergy Asthma Rep. 2014; 14: 437.
5. Neves MC, Neves YC, Mendes CM, Bastos MN, Camelier AA, Queiroz CF, Mendoza BF, Lemos AC, D’Oliveira Junior A. Evaluation of atopy in patients with COPD. J Bras Pneumol. 2013; 39: 296–305.
6. Fattahi F, ten Hacken NH, Löfdahl CG, Hylkema MN, Timens W, Postma DS,Vonk JM. Atopy is a risk factor for respiratory symptoms in COPD patients: results from the EUROSCOP study. Respir Res. 2013; 28 (14):10.
7. Braman SS. The chronic obstructive pulmonary disease-asthma overlap syndrome. Allergy Asthma Proc. 2015; 36: 11–8.
8. Heinzerling LM, Burbach GJ, Edenharter G, Bachert C, Bindslev-Jensen C, Bonini S, et al. GA(2)LEN skin test study I: GA(2)LEN harmonization of skin prick testing: novel sensitization patterns for inhalant allergens in Europe. Allergy. 2009; 64: 1498–1506.
9. Hizawa N. Clinical approaches towards asthma and chronic obstructive pulmonary disease based on the heterogeneity of disease pathogenesis. Clin Exp Allergy. 2016; 46: 678–87.
10. Ichinose M. Differences of inflammatory mechanisms in asthma and COPD. Allergol Int. 2009; 58: 307–13.
11. Li BW, Hendriks RW. Group 2 innate lymphoid cells in lung inflammation. Immunology. 2013; 140: 281–287.
12. Tsai JJ, Liao EC, Hsu JY, Lee WJ, Lai YK. The differences of eosinophil-and neutrophil-related inflammation in elderly allergic and non-allergic chronic obstructive pulmonary disease. J Asthma. 2010; 47: 1040–4.
13. Ogershok PR, Warner DJ, Hogan MB, Wilson NW. Prevalence of pollen sensitization in younger children who have asthma. Allergy Asthma Proc. 2007; 28: 654–658.
14. Pawankar R, Canonica GW, Holgate ST, Lockey RF. Allergic diseases and asthma: a major global health concern. Curr Opin Allergy Clin Immunol. 2012; 12: 39–41.
15. Simpson CR, Anderson WJ, Helms PJ, Taylor MW, Watson L, Prescott GJ, Godden DJ, Barker RN. Coincidence of immune-mediated diseases driven by Th1 and Th2 subsets suggests a common aetiology. A population-based study using computerized general practice data. Clin Exp Allergy. 2002; 32: 37–42.
16. Holt PG, Sly PD. Non-atopic intrinsic asthma and the ‘family tree’ of chronic respiratory disease syndromes. Clin Exp Allergy. 2009; 39: 807–11.
17. Ngoc PL, Gold DR, Tzianabos AO, Weiss ST, Celedón JC. Cytokines, allergy, and asthma. Curr Opin Allergy Clin Immunol. 2005; 5; 161–166.
18. Shirai T, Inui N, Suda T, Chida K. Correlation between peripheral blood T-cell profiles and airway inflammation in atopic asthma. J Allergy Clin Immunol. 2006; 118: 622–6.
19. Schoenborn JR, Wilson CB. Regulation of interferon-gamma during innate and adaptive immune responses. Adv Immunol. 2007; 96: 41–101.
20. Liao W, Lin JX, Leonard WJ. IL-2 family cytokines: new insights into the complex roles of IL-2 as a broad regulator of T helper cell differentiation. Curr Opin Immunol. 2011; 23: 598–604.
21. Malek TR, Castro I. Interleukin-2 receptor signaling: at the interface between tolerance and immunity. Immunity 2010; 27:153–65.
22. Perkins PC, Wills-Karp M, Finkelman FD. IL-4 induces IL-13-independent allergic airway inflammation. J Allergy Clin Immunol. 2006; 118: 410–9.
eISSN:1898-2263
ISSN:1232-1966