A murine model of stress controllability attenuates Th2-dominant airway inflammatory responses

被引:8
作者
Deshmukh, Aniket [1 ]
Kim, Byung-Jin [1 ]
Gonzales, Xavier [1 ]
Caffrey, James [2 ]
Vishwanatha, Jamboor [1 ]
Jones, Harlan P. [1 ]
机构
[1] Univ N Texas, Hlth Sci Ctr, Dept Mol Biol & Immunol, Ft Worth, TX 76107 USA
[2] Univ N Texas, Hlth Sci Ctr, Dept Integrat Physiol, Ft Worth, TX 76107 USA
关键词
Stress; Controllability; Asthma; Immunity; LEARNED HELPLESSNESS; T-LYMPHOCYTES; CELLS; DYSREGULATION; ACTIVATION; PHENOTYPE; HEALTH; ASTHMA; IMPACT; STATES;
D O I
10.1016/j.jneuroim.2010.03.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Epidemiological and experimental studies suggest a positive correlation between chronic respiratory inflammatory disease and the ability to cope with adverse stress. Interactions between neuroendocrine and immune systems are believed to provide insight toward the biological mechanisms of action. The utility of an experimental murine model was employed to investigate the immunological consequences of stress-controllability and ovalbumin-induced airway inflammation. Pre-conditioned uncontrollable stress exacerbated OVA-induced lung histopathological changes that were typical of Th2-predominant inflammatory response along respiratory tissues. Importantly, mice given the ability to exert control over aversive stress attenuated inflammatory responses and reduced lung pathology. This model represents a means of investigating the neuro-immune axis in defining mechanisms of stress and respiratory disease. (C) 2010 Elsevier BM. All rights reserved.
引用
收藏
页码:13 / 21
页数:9
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