Inhibition of high-mobility group box 1 in lung reduced airway inflammation and remodeling in a mouse model of chronic asthma
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- 作者：Chen-Chen Lee ; Yu-Ting Lai ; Hao-Teng Chang ; Jiunn-Wang Liao ; Woei-Cherng Shyu ; Chi-Yuan Li ; Chien-Neng Wang
- 关键词：HMGB1 ; Airway inflammation ; Airway remodeling ; IL-17
- 刊名：Biochemical Pharmacology
- 出版年：2013
- 出版时间：1 October, 2013
- 年：2013
- 卷：86
- 期：7
- 页码：940-949
- 全文大小：3517 K
文摘
The role of high-mobility group box 1 (HMGB1) in chronic allergic asthma is currently unclear. Both airway neutrophilia and eosinophilia and increase in HMGB1 expression in the lungs in our murine model of chronic asthma. Inhibition of HMGB1 expression in lung in ovalbumin (OVA)-immunized mice decreased induced airway inflammation, mucus formation, and collagen deposition in lung tissues. Analysis of the numbers of CD4+ T helper (Th) cells in the mediastinal lymph nodes and lungs revealed that Th17 showed greater increases than Th2 cells and Th1 cells in OVA-immunized mice; further, the numbers of Th1, Th2, and Th17 cells decreased in anti-HMGB1 antibody (Ab)-treated mice. In OVA-immunized mice, TLR-2 and TLR-4 expression, but not RAGE expression, was activated in the lungs and attenuated after anti-HMGB1 Ab treatment. The results showed that increase in HMGB1 release and expression in the lungs could be an important pathological mechanism underlying chronic allergic asthma and HMGB1 might a potential therapeutic target for chronic allergic asthma.