IL-23 Gene and Protein Expression in Childhood Asthma.
نویسندگان
چکیده
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 adult allergic 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.
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IL-23 Gene and Protein Expression in Childhood Asthma
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...
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ورودعنوان ژورنال:
- Iranian journal of immunology : IJI
دوره 14 1 شماره
صفحات -
تاریخ انتشار 2017