| First Author | Rabolli V | Year | 2014 |
| Journal | J Biol Chem | Volume | 289 |
| Issue | 20 | Pages | 13937-47 |
| PubMed ID | 24700466 | Mgi Jnum | J:214123 |
| Mgi Id | MGI:5588084 | Doi | 10.1074/jbc.M113.534594 |
| Citation | Rabolli V, et al. (2014) Critical role of aquaporins in interleukin 1beta (IL-1beta)-induced inflammation. J Biol Chem 289(20):13937-47 |
| abstractText | Rapid changes in cell volume characterize macrophage activation, but the role of water channels in inflammation remains unclear. We show here that, in vitro, aquaporin (AQP) blockade or deficiency results in reduced IL-1beta release by macrophages activated with a variety of NLRP3 activators. Inhibition of AQP specifically during the regulatory volume decrease process is sufficient to limit IL-1beta release by macrophages through the NLRP3 inflammasome axis. The immune-related activity of AQP was confirmed in vivo in a model of acute lung inflammation induced by crystals. AQP1 deficiency is associated with a marked reduction of both lung IL-1beta release and neutrophilic inflammation. We conclude that AQP-mediated water transport in macrophages constitutes a general danger signal required for NLRP3-related inflammation. Our findings reveal a new function of AQP in the inflammatory process and suggest a novel therapeutic target for anti-inflammatory therapy. |
