Affiliation:
1. Department of General and Oncological Pulmonology, Medical University of Lodz, Lodz, Poland
2. Department of Molecular Bases of Medicine, Medical University of Lodz, Lodz, Poland
3. Department of Pneumonology and Allergy, 1st Chair of Internal Diseases, Medical University of Lodz, Lodz, Poland
Abstract
Introduction: Asthma is associated with activation of interleukin-4 (IL-4)/interleukin-13 (IL-13)/signal transducer and activator of transcription factor-6(STAT6) inflammatory response via overexpression of all pathway components: IL-4, IL-13, and STAT6. Objectives: To evaluate the association of IL-4, IL-13, and STAT6 expression and immunoexpression with atopic asthma development. Patients and methods: Fifty patients with atopic asthma and 20 healthy controls were enrolled into the study. Relative gene expression was analyzed by qPCR method. Immunoexpression was assessed by ELISA method. Results: The expression levels of IL-4, IL-13, and STAT6 were higher in patients compared to the controls, but a statistically significant difference was observed only for IL-13 ( P = 0.03). In immunoexpression analysis, a statistically significant difference between patients and controls was found for IgE ( P = 0.03). Significant positive correlations in the patient group were found between IL-13 gene expression and total level of serum IgE (rho = 0.230, P = 0.033), STAT6 gene/STAT6 protein and total level of serum IgE ( STAT6: rho = 0.077, P = 0.038; STAT6: rho = 0.049, P = 0.042), IL-4, and STAT6 expression (rho = 0.098, P = 0.048). Any significant correlations were found between expression/immunoexpression levels of the studied genes and clinical classification, clinical features, or lung function parameters. Conclusions: Our data support the role of Th2 cytokines (IL-4, IL-13) and STAT6 in Th1/Th2 imbalance and highlight the etiological relationship between IL-4/IL-13/STAT6 signaling and atopy and asthma.
Subject
Pharmacology,Immunology,Immunology and Allergy
Cited by
23 articles.
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