| First Author | Zhang WC | Year | 2015 |
| Journal | Cell Res | Volume | 25 |
| Issue | 8 | Pages | 893-910 |
| PubMed ID | 26206316 | Mgi Jnum | J:302711 |
| Mgi Id | MGI:6509507 | Doi | 10.1038/cr.2015.87 |
| Citation | Zhang WC, et al. (2015) High salt primes a specific activation state of macrophages, M(Na). Cell Res 25(8):893-910 |
| abstractText | 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 proendocytic 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 Erk1/2/cFos pathways, while inhibited the anti-inflammatory and proendocytic aspects by Erk1/2/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). |
