High salt primes a specific activation state of macrophages, M（Na）

High salt is positively associated with the risk of many diseases. However, little is known about the mechanisms. Here we showed that high salt increased proinflammatory molecules, while decreased anti-inflammatory and pro- endocytic molecules in both human and mouse macrophages. High salt also pote...

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Bibliographic Details
Published in细胞研究：英文版 no. 8; pp. 893 - 910
Main Author Wu-Chang Zhang Xiao-Jun Zheng Lin-Juan Du Jian-Yong Sun Zhu-Xia Shen Chaoji Shi Shuyang Sun Zhiyuan Zhang Xiao-qing Chen Mu Qin Xu Liu Jun Tao Lijun Jia Heng-yu Fan Bin Zhou Ying Yu Hao Ying Lijian Hui Xiaolong Liu Xianghua Yi Xiaojing Liu Lanjing Zhang Sheng-Zhong Duan
Format Journal Article
LanguageEnglish
Published 2015
Subjects
小鼠巨噬细胞
活化状态
白细胞介素4
细胞特异性
肺泡巨噬细胞
转录激活因子
高盐
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Summary:High salt is positively associated with the risk of many diseases. However, little is known about the mechanisms. Here we showed that high salt increased proinflammatory molecules, while decreased anti-inflammatory and pro- endocytic molecules in both human and mouse macrophages. High salt also potentiated lipopolysaccharide-induced macrophage activation and suppressed interleukin 4-induced macrophage activation. High salt induced the proinflammatory aspects by activating p38/cFos and/or Erkl/2/cFos pathways, while inhibited the anti-inflammatory and proendocytic aspects by Erkl/2/signal transducer and activator of transcription 6 pathway. Consistent with the in vitro results, high-salt diet increased proinflammatory gene expression of mouse alveolar macrophages. In mouse models of acute lung injury, high-salt diet aggravated lipopolysaccharide-induced pulmonary macrophage activation and inflammation in lungs. These results identify a novel macrophage activation state, M（Na）, and high salt as a potential environmental risk factor for lung inflammation through the induction of M（Na）.
Bibliography:High salt is positively associated with the risk of many diseases. However, little is known about the mechanisms. Here we showed that high salt increased proinflammatory molecules, while decreased anti-inflammatory and pro- endocytic molecules in both human and mouse macrophages. High salt also potentiated lipopolysaccharide-induced macrophage activation and suppressed interleukin 4-induced macrophage activation. High salt induced the proinflammatory aspects by activating p38/cFos and/or Erkl/2/cFos pathways, while inhibited the anti-inflammatory and proendocytic aspects by Erkl/2/signal transducer and activator of transcription 6 pathway. Consistent with the in vitro results, high-salt diet increased proinflammatory gene expression of mouse alveolar macrophages. In mouse models of acute lung injury, high-salt diet aggravated lipopolysaccharide-induced pulmonary macrophage activation and inflammation in lungs. These results identify a novel macrophage activation state, M（Na）, and high salt as a potential environmental risk factor for lung inflammation through the induction of M（Na）.
high salt; macrophage activation; acute lung injury
31-1568
ISSN:1001-0602
1748-7838