Reza Yazdani , Mazdak Ganjalikhani Hakemi, Roya Sherkat , Abbas Rezaei , Rahim Farahani , Behrouz Beiranvand ,
Volume 72, Issue 9 (12-2014)
Abstract
Background: Asthma as an airway disease is identified by increase network respon-siveness of the trachea and bronchus to a specific stimulus. Th17 cells through produc-tion of IL-17 have important role in inflammation and autoimmune diseases .In some studies has been shown which IL-17 as major cytokine of Th17 probably has im-portant role in the pathogenesis of allergy and asthma.
Methods: Total mRNA extracted from whole blood samples and sputum of 23 asthma patients and 23 normal controls. Then, total RNA was converted into cDNA according to the manufacturer’s instructions. Finally, the transcript levels of IL-17 were quanti-fied by the real-time quantitative PCR. Twenty-three patients with asthma were diag-nosed and selected according to the global initiative for asthma (GINA) and none of the patients had taken the medication at least three week before sampling. Healthy in-dividuals did not have any history of allergy, asthma and other inflammatory diseases at the time of sampling. All of experiments have done in Isfahan University of Medical Sciences, Iran during May to February, 2013.
Results: This study showed a significant increase in transcript levels of IL-17 in the blood (287±79 versus 1/18±0/13) and sputum samples of the patients (64±28 versus 0/9±0/1) in comparison with normal individuals (P= 0.000, P= 0.029 respectively). It al-so revealed that the expression levels of the cytokines in the serum samples of the asthmatics were significantly more than their levels in patient’s sputum samples (P= 0.000). However, there was no significant difference between the cytokines expression levels in serum samples and sputum samples of the controls (P> 0.05).
Conclusion: In this study, we showed which the expression of IL-17 was increased in serum and sputum of asthmatic patients compared to healthy controls, this could re-sult in elevation of neutrophils population and activation of pulmonary neutrophil.