HMGB1 regulates IL-33 expression in acute respiratory distress syndrome
HMGB1 regulates IL-33 expression in acute respiratory distress syndrome
复制标题
HMGB1 调节急性呼吸窘迫综合征中 IL-33 的表达
DOI：
10.1016/j.intimp.2016.06.010
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发表时间：
2016-09-01
影响因子：
5.6
通讯作者：
Xu, Fang
中科院分区：
文献类型：
--
作者：
Fu, Juan;Lin, Shi-hui;Xu, Fang
急性呼吸窘迫综合征（ARDS）的发生和发展受到细胞因子的调节。IL-33和HMGB 1通常被认为是核蛋白，具有促炎作用。已有研究证实HMGB 1在ARDS中具有重要作用，但很少有研究提供直接证据证实HMGB 1参与了ARDS。本研究的目的是探讨IL-33在ARDS中的表达及其与HMGB 1的关系。我们建立了LPS诱导的肺部炎症/损伤的小鼠模型。取血清、支气管肺泡灌洗液（BALF）和肺组织测定相关指标。与对照组相比，LPS给药后24 h，血清、CALF和肺中的IL-33水平均显著升高。我们还发现血清和支气管肺泡灌洗液中的HMGB 1和其他Th 1细胞因子/趋化因子水平也明显升高，但血清和支气管肺泡灌洗液中的Th 2细胞因子水平没有增加。为了进一步研究IL-33和HMGB 1之间的关系，在LPS给药之前，用HMGB 1抑制剂（alcohol in）预处理小鼠。结果表明，IL-33和HMGB 1的表达明显低于LPS组，肺损伤明显减轻。血清和BALF中其他Th 1细胞因子和趋化因子水平也显著降低。结果表明，IL-33可能是ARDS的一个重要因素，HMGB 1的释放可能与IL-33表达上调有关。(C)2016爱思唯尔B. V.保留所有权利。
The development and progression of acute respiratory distress syndrome (ARDS) has been shown to be regulated by cytokines. IL-33 and HMGB1 are conventionally considered as nuclear proteins and have a proinflammatory role. Studies have confirmed that HMGB1 has a significant role in ARDS, but few studies have provided direct evidence to confirm that 1133 is involved in ARDS. The purpose of our study was to determine whether IL-33 is elevated in ARDS and the relationship between IL-33 and HMGB1 in ARDS. We established a mouse model of LPS-induced lung inflammation/injury. Serum, bronchoalveolar lavage fluid (BALF) and lung tissues were obtained to determine the related indicators. IL-33 levels in both the serum, CALF and lungs were significantly increased at 24 h after LPS administration compared to the control group. We also found that HMGB1 and other Th1 cytokine/chemokine levels in serum and BALF were also significantly elevated, but the Th2 cytokine levels in serum and BALF didn't increase. To further study the relationship between IL-33 and HMGB1, mice were pretreated with glycyrrhizin (an inhibitor of HMGB1) prior to LPS administration. We found that the expression of IL-33 and HMGB1 were markedly lower than those in the LPS group and the lung injury was ameliorated. The levels of other Th1 cytokines and chemokines in serum and BALF were also significantly decreased. The results showed that IL-33 is, likely a major factor in ARDS, and the release of HMGB1 may be correlated with up-regulation of IL-33 expression. (C) 2016 Elsevier B.V. All rights reserved.