Abstract
To investigate the expression and its significance of interleutin-17 (IL-17) and immunoglobulin E (IgE) in patients with bronchial asthma, sixty adult patients with bronchial asthma and 30 healthy human control were sequentially enrolled in this study. The production of IL-17 was measured by enzyme-linked immunosorbent assay (ELISA) and fluorescent quantitative polymerase chain reaction (qPCR), respectively. The correlation between expression of IgE and IL-17 was analyzed. It was found that IL-17 was significantly up-regulated in bronchial asthma in comparison to the health control on mRNA level, and serum levels of IL-17 and IgE in bronchial asthma were significantly higher than those in health control, respectively (P < 0. 001). Significant positive correlation in bronchial asthma were found between expression of IL-17 and IgE (r = 0.7082, P = 0.0418). The present study implied that expressions of IL-17 and IgE play an important role in the development of bronchial asthma. Key words: Bronchial asthma, immunoglobulin E, interleukin-17, enzyme-linked immunosorbent assay (ELISA).
Highlights
Bronchial asthma is one of the most common chronic inflammatory diseases affecting children and young adults and has high morbidity and mortality (Anderson, 2008; Lemanske et al, 2010), and increased total serum immunoglobulin E (IgE) levels (Boushey et al, 1980; Burrows et al, 1989; Kashiwakura et al, 2011), both of which have a strong genetic component (Marsh et al, 1981; Hopp et al, 1990; Postma et al, 1995; Xu et al, 2000; Palm et al, 2012 )
In order to detect the mRNA expression of IL-17 in patients with bronchitis asthma, fluorescent quantitative RT-polymerase chain reaction (PCR) was conducted
The IL-17 protein expression levels in bronchitis asthma group were significantly up-regulated as compared to health control group (P
Summary
Bronchial asthma is one of the most common chronic inflammatory diseases affecting children and young adults and has high morbidity and mortality (Anderson, 2008; Lemanske et al, 2010), and increased total serum immunoglobulin E (IgE) levels (Boushey et al, 1980; Burrows et al, 1989; Kashiwakura et al, 2011), both of which have a strong genetic component (Marsh et al, 1981; Hopp et al, 1990; Postma et al, 1995; Xu et al, 2000; Palm et al, 2012 ) These features stem largely from the actions of CD4+ Th2 cells, which produce the cytokines IL-4, IL-5, and IL-13 and thereby promote IgE production, eosinophilia, and mucus secretion into the airway (Herrick et al, 2003; Larche et al, 2003). An improved understanding of the cellular and molecular mechanisms that regulate TH2 and TH17 effector responses might lead to novel therapeutic strategies to prevent or control bronchial asthma
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