RU486 blocks the anti-inflammatory effects of exercise in a murine model of allergen-induced pulmonary inflammation
- 作者：Amy Pastva ; Kim Estell ; Trenton R. Schoeb and Lisa M. Schwiebert
- 关键词：Exercise ; Asthma ; Inflammation ; Glucocorticoids ; RU486 ; NF-κ ; B
- 刊名：Brain ; Behavior ; and Immunity
- 出版年：2005
- 期刊代码：79_08891591
- 类别：psy
- 出版时间：2005
- 卷：19
- 期：5
- 页码：413-422
- 文件大小：717 K
摘要
In an ovalbumin (OVA)-driven murine model of allergic pulmonary inflammation, we have shown previously that moderate-intensity aerobic exercise training attenuates inflammatory responses, disease progression, and NF-κB activation within the sensitized lung. Glucocorticoids (GCs), potent anti-inflammatory agents, have been shown to alter transcriptional events that are important in asthmatic pathogenesis, such as NF-κB activation. Notably, exercise training can alter the production and signaling capacity of endogenous GCs. Because GCs exert their anti-inflammatory effects through binding to intracellular glucocorticoid receptors (GRs), we examined the role of the GR in facilitating the anti-inflammatory effects of exercise. Results show that, in exercised OVA-sensitized mice, treatment with the GR antagonist RU486 blocked the exercise-induced reductions in cellular infiltration of the airways (p < .05), KC and soluble VCAM-1 protein levels in the bronchoalveloar lavage fluid (p < .05), and NF-κB translocation and DNA binding within the lung to levels similar to those observed in sedentary OVA-sensitized mice. Importantly, RU486 treatment also blocked exercise-induced increases in GR nuclear translocation to the levels seen in sensitized control mice. Together, these results suggest that GR nuclear translocation and NF-κB activation play roles in mediating the anti-inflammatory effects of exercise in allergen-mediated lung pathology.