Lipopolysaccharide-induced CCN1 production enhances interleukin-6 secretion in bronchial epithelial cells.
Lipopolysaccharide-induced CCN1 production enhances interleukin-6 secretion in bronchial epithelial cells.
复制标题
脂多糖诱导的 CCN1 产生增强支气管上皮细胞中白细胞介素 6 的分泌
DOI：
10.1007/s10565-017-9401-1
复制
发表时间：
2018-03
影响因子：
6.1
通讯作者：
Chen C
中科院分区：
文献类型：
--
作者：
Shi L;Dong N;Ji D;Huang X;Ying Z;Wang X;Chen C
急性肺损伤/急性呼吸窘迫综合征（ALI/ARDS）是由原发性或继发性肺损伤以及全身性炎症引起的临床并发症。关于ALI/ARD的分子病理生理学的研究正在浸入最终的目的，目的是开发预后的分子生物标志物和基于分子的疗法。但是，关于ALI/ARD的分子机制仍未完全了解。本研究的目的是确定CCN1在ALI/ARDS期间炎症微环境中的关键作用，并专注于气道上皮细胞中CCN1和白介素6（IL-6）之间的潜在通信。我们的数据表明，在脂多糖（LPS）诱导的ALI小鼠模型中，CCN1和IL-6的表达水平显着升高，CCN1的肺表达限制为支气管上皮细胞。有趣的是，内源性和外源性CCN1均在体外刺激了IL-6产生。此外，在支气管上皮细胞系中LPS诱导的IL-6产生被CCN siRNA阻断，而LPS诱导的CCN1对PI3K抑制敏感。总之，我们的数据表示LPS暴露后的支气管上皮细胞中存在线性信号途径LPS-CCN1-IL-6。这一发现可能代表了在ALI/ARDS上开发治疗和生物标志物开发的额外机制和新颖的目标。
本文的在线版本（DOI：10.1007/S10565-017-9401-1）包含补充材料，可供授权用户使用。
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a clinical complication caused by primary or secondary lung injury, as well as by systemic inflammation. Researches regarding molecular pathophysiology of ALI/ARDS are immerging with an ultimate aim towards developing prognostic molecular biomarkers and molecule-based therapy. However, the molecular mechanisms concerning ALI/ARDS are still not completely understood. The purpose of the present study was to identify a crucial role of CCN1 in inflammatory microenvironment during ALI/ARDS and focus on a potential communication between CCN1 and interleukin-6 (IL-6) in the airway epithelial cells. Our data illustrated that the expression levels of CCN1 and IL-6 in bronchoalveolar lavage fluid (BALF) in a lipopolysaccharide (LPS)-induced ALI mouse model were significantly elevated and the pulmonary expression of CCN1 was restricted to bronchial epithelial cells. Interestingly, both endogenous and exogenous CCN1 stimulated IL-6 production in vitro. Furthermore, LPS-induced IL-6 production in a bronchial epithelial cell line was blocked by CCN siRNA whereas CCN1 induced by LPS was sensitive to PI3K inhibition. Together, our data indicate a linear signal pathway, LPS-CCN1-IL-6, existing in bronchial epithelial cells after LPS exposure. This finding may represent an additional mechanism and a novel target for development of therapy and biomarker on ALI/ARDS.
登录
查看更多内容
影响因子：
9.6
作者：
Chen, Chengshui;Fang, Xiaocong;Wang, Xiangdong
通讯作者：
Wang, Xiangdong
影响因子：
5.8
作者：
Wallace MJ;Probyn ME;Zahra VA;Crossley K;Cole TJ;Davis PG;Morley CJ;Hooper SB
通讯作者：
Hooper SB
影响因子：
21.3
作者：
Jun, Joon-Il;Lau, Lester F.
通讯作者：
Lau, Lester F.
DOI：
10.1152/ajplung.00190.2014
发表时间：
2015-04-15
影响因子：
4.9
作者：
Grazioli, Serge;Gil, Sucheol;Matute-Bello, Gustavo
通讯作者：
Matute-Bello, Gustavo
DOI：
10.1165/rcmb.2005-0144oc
发表时间：
2005-09-01
影响因子：
6.4
作者：
Jin, Y;Kim, HP;Choi, AMK
通讯作者：
Choi, AMK