Expression of Interleukin-17 in Lung and Peripheral Blood of Asthmatic Rats and the Influence of Dexamethasone
- Author:
Weining XIONG
1
;
Daxiong ZENG
;
Yongjian XU
;
Huijuan FANG
;
Yong CAO
;
Qingfeng SONG
;
Chao CAO
Author Information
1. 华中科技大学同济医学院附属同济医院
- Keywords:
bronchial asthma;
interleukin-17;
pathogenesis
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2007;27(5):498-500
- CountryChina
- Language:Chinese
-
Abstract:
The expression of interleukin-17 (IL-17) in lung and peripheral blood of asthmatic rats and the influence of dexamethasone, and the role of IL-17 in the pathogenesis of asthma were inves-tigated. Thirty Sprague-Dawley (SD) adult rats were randomly divided into three groups (n=10 in each group): normal group, asthmatic group, and dexamethasone-interfered group. Rat asthmatic model was established by intraperitoneal (I.p.) injection of 10% ovalbumin (OVA) and challenge with 1% OVA via inhalation. Rats in dexamethasone-interfered group were pretreated with dexa-methasone (2 mg/kg, I.p.) 30 rain before each challenge. The expression of IL-17 protein in serum and bronchoalveolar lavage fluid (BALF) was detected by ELISA. The expression of IL-17 mRNA in peripheral blood mononuclear cells (PBMC) and BALF cells was semi-quantitatively detected by RT-PCR. The expression of IL-17 protein in serum and BALF of asthmatic rats was significantly elevated as compared with normal rats and dexamethsone-interfered rats (P<0.01), and there was sig- nificant difference between normal rats and dexamethsone-interfered rats (P<0.05). The expression of IL-17 mRNA in PBMC and BALF cells of asthmatic rats was markedly increased as compared with normal rats and dexamethsone-interfered rats (P<0.01), and significant difference was found between normal rats and dexamethsone-interfered rats (P<0.05). It was concluded that the expression of IL-17 was increased significantly in asthmatic rats and could be inhibited partly by dexamethasone, sug-gesting that IL-17 might play an important role in the pathogenesis of asthma as an inflammation regulation factor.
