Impact of psychosocial stress on airway inflammation and its mechanism in a mUrine model of allergic asthma  

作　　者：LI Bei DUAN Xiao-hong WU Jin-feng LIU Bao-jun LUO Qing-li JIN Hua-liang DU Yi-jie ZHANG Hong-ying CAO Yu-xue DONG Jing-cheng 

机构地区：[1]Department of Integrative Medicine, Huashan Hospital, FudanUniversity, Shanghai 200040, China

出　　处：《Chinese Medical Journal》2013年第2期325-334,共10页中华医学杂志（英文版）

摘　　要：Background It has already been recognized that psychosocial stress evokes asthma exacerbation; however, the mechanism of how stress gets inside the body is not clear. This study aimed to observe the impact of psychosocial stress on airway inflammation and its mechanism in the ovalbumin-induced asthmatic mice combined with social disruption stress. Methods Thirty-six male BALB/c mice were randomly divided into： control group, asthma group （ovalbumin-induced）, asthma plus social disruption stress group （SDR）, and SDR group. The open field video tracking system was used to assess animal behaviors. The invasive pulmonary resistance （RL） and dynamic lung compliance （cdyn） test system from Buxco was applied to detect pulmonary function. The enzyme-linked immunosorbent assay （ELISA） was utilized to determine OVA-IgE, T-helper type 2 （Th2） cytokines （IL-4, IL-5, IL-13） and corticosterone in mouse serum, the Th2 cytokines （IL-4, IL-5, IL-13, IL-6, TNF-a） in bronchoalveolar lavage fluid （BALF）, and IL-6 and TNF-a levels in the supernatant of splenocytes cultured in vitro. Hematoxylin-eosin （H＆E） staining was used to assess airway inflammation in lung histology. The cell count kit-8 assay （CCK-8） was applied to evaluate the inhibitory effect of corticosterone on splenocyte proliferation induced by lipopolysacchadde （LPS）. Real time-PCR and Western blotting were utilized to determine glucocorticoid receptor （GR） mRNA and GR protein expression in lungs. Results The open field test showed that combined allergen exposure and repeated stress significantly shortened the time the mice spent in the center of the open field （P 〈0.01）, increased ambulatory activity （P 〈0.01） and the count of fecal boli （P 〈0.01）, but deceased vertical activity （P 〈0.01）. Results from pulmonary function demonstrated that airway hyperresponsiveness （AHR） was enhanced by psychosocial stress compared with allergy exposure alone. The ELISA results showed that cytokines in Background It has already been recognized that psychosocial stress evokes asthma exacerbation; however, the mechanism of how stress gets inside the body is not clear. This study aimed to observe the impact of psychosocial stress on airway inflammation and its mechanism in the ovalbumin-induced asthmatic mice combined with social disruption stress. Methods Thirty-six male BALB/c mice were randomly divided into： control group, asthma group （ovalbumin-induced）, asthma plus social disruption stress group （SDR）, and SDR group. The open field video tracking system was used to assess animal behaviors. The invasive pulmonary resistance （RL） and dynamic lung compliance （cdyn） test system from Buxco was applied to detect pulmonary function. The enzyme-linked immunosorbent assay （ELISA） was utilized to determine OVA-IgE, T-helper type 2 （Th2） cytokines （IL-4, IL-5, IL-13） and corticosterone in mouse serum, the Th2 cytokines （IL-4, IL-5, IL-13, IL-6, TNF-a） in bronchoalveolar lavage fluid （BALF）, and IL-6 and TNF-a levels in the supernatant of splenocytes cultured in vitro. Hematoxylin-eosin （H＆E） staining was used to assess airway inflammation in lung histology. The cell count kit-8 assay （CCK-8） was applied to evaluate the inhibitory effect of corticosterone on splenocyte proliferation induced by lipopolysacchadde （LPS）. Real time-PCR and Western blotting were utilized to determine glucocorticoid receptor （GR） mRNA and GR protein expression in lungs. Results The open field test showed that combined allergen exposure and repeated stress significantly shortened the time the mice spent in the center of the open field （P 〈0.01）, increased ambulatory activity （P 〈0.01） and the count of fecal boli （P 〈0.01）, but deceased vertical activity （P 〈0.01）. Results from pulmonary function demonstrated that airway hyperresponsiveness （AHR） was enhanced by psychosocial stress compared with allergy exposure alone. The ELISA results showed that cytokines in

关 键 词：psychosocial stress  asthma  glucocorticoid insensitivity glucocorticoid receptor 

分 类 号：S853.9[农业科学—临床兽医学] TS218[农业科学—兽医学]