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IL-23 Gene and Protein Expression in Childhood Asthma
- Source :
- Iranian Journal of Immunology, Vol 14, Iss 1, Pp 73-80 (2017)
- Publication Year :
- 2017
- Publisher :
- Shiraz University of Medical Sciences, 2017.
-
Abstract
- Background: Asthma is the chronic inflammation of airways characterized by eosinophilic infiltration, mucus overproduction, airway hyper-responsiveness and airway remodeling. These changes are induced mostly by cytokines which are produced by T helper (Th) 2 cells. Recently, the role of interleukin-23 (IL-23) in the pathogenesis of adultallergic asthma has been studied. Objective: To explore IL-23 serum levels and its expression in persistent asthma compared with healthy children younger than five years old. Method: Blood samples of 40 children with mild and severe persistent asthma were compared to 34 healthy children regarding IL-23 serum levels and gene expression using enzyme-linked immunosorbentassay (ELISA) and real time quantitative polymerase chain reaction (PCR). Results: The IL-23 gene expression level was significantly different in the 25 children with mild persistent asthma and the 15 children with severe persistent asthma compared to the control group (p=0.001).There was no significant difference in IL-23 gene expression level between the two groups of patients with mild and severe persistent asthma. A significant difference was seen in IL-23 serum levels between the 25 children with persistent asthma and control group (p=0.002).Conclusion: For pre-school children with history and physical exam in favor of asthma which cannot be tested by spirometry, IL-23 serum levels may be an auxiliary biomarker for the diagnosis of asthma.
- Subjects :
- Asthma
Childhood
Interleukin-23
Biology (General)
QH301-705.5
Subjects
Details
- Language :
- English
- ISSN :
- 17351383 and 1735367X
- Volume :
- 14
- Issue :
- 1
- Database :
- Directory of Open Access Journals
- Journal :
- Iranian Journal of Immunology
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.572ec0e2af0b494ebfdd3572e35d9702
- Document Type :
- article