Protective effect of resolvin E1 on the development of asthmatic airway inflammation

被引:70
作者
Aoki, Haruka [1 ]
Hisada, Takeshi [1 ]
Ishizuka, Tamotsu [1 ]
Utsugi, Mitsuyoshi [1 ]
Ono, Akihiro [1 ]
Koga, Yasuhiko [1 ]
Sunaga, Noriaki [1 ]
Nakakura, Takashi [2 ]
Okajima, Fumikazu [2 ]
Dobashi, Kunio [3 ]
Mori, Masatomo [1 ]
机构
[1] Gunma Univ, Grad Sch Med, Dept Med & Mol Sci, Maebashi, Gunma 3718511, Japan
[2] Gunma Univ, Inst Mol & Cellular Regulat, Lab Signal Transduct, Maebashi, Gunma 3718512, Japan
[3] Gunma Univ, Sch Hlth Sci, Maebashi, Gunma 3718511, Japan
关键词
Bronchial asthma; Lipid mediator; Resolvin; Airway hyperresponsiveness; Airway inflammation; CD8(+) T-CELLS; DENDRITIC CELLS; HYPERRESPONSIVENESS; RECEPTOR-1; RESOLUTION;
D O I
10.1016/j.bbrc.2010.08.025
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Resolvin E1 (RvE1) is an anti-inflammatory lipid mediator derived from the omega-3 fatty acid eicosapentaenoic acid (EPA), and strongly acts in the resolution of inflammation. We previously reported that RvE1 dampens airway inflammation and hyperresponsiveness in a murine model of asthma. In the present study, to elucidate the effects of RvE1 on the development of asthmatic airway inflammation, we investigated whether RvE1 acts on different phases of an OVA-sensitized and -challenged mouse model of asthma. RvE1 treatments at the time of either OVA sensitization or at the time of OVA challenge were investigated and compared with RvE1 treatments at the time of both OVA sensitization and challenge. After RvE1 was administered to mice intraperitoneally at the time of both OVA sensitization and challenge, there were decreases in airway eosinophil and lymphocyte recruitment, as well as a reduction in Th2 cytokine and airway hyperresponsiveness. RvE1 treatment at the time of either OVA sensitization or challenge also improved AHR and airway inflammation. Our results suggest that RvE1 acts on several phases of asthmatic inflammation and may have anti-inflammatory effects on various cell types. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:128 / 133
页数:6
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