| First Author | Wallace DF | Year | 2015 |
| Journal | Int Immunol | Volume | 27 |
| Issue | 6 | Pages | 281-7 |
| PubMed ID | 25568302 | Mgi Jnum | J:230915 |
| Mgi Id | MGI:5766446 | Doi | 10.1093/intimm/dxu144 |
| Citation | Wallace DF, et al. (2015) Analysis of IL-22 contribution to hepcidin induction and hypoferremia during the response to LPS in vivo. Int Immunol 27(6):281-7 |
| abstractText | The anaemia of chronic disease (ACD) results from inflammation-mediated up-regulation of the iron regulatory hormone hepcidin, with the consequent sequestration of iron limiting its availability for erythropoiesis. The inflammatory cytokine IL-6, a regulator of hepcidin, has been implicated in this process. Recent in vivo and in vitro studies indicate that IL-22 is also able to stimulate hepcidin expression. We aimed to determine if IL-22 had a role in causing the hypoferremia associated with the inflammatory response. Wild-type and Il22-knockout mice were subjected to an acute inflammatory stimulus via administration of LPS and the response of hepcidin and iron homeostasis was analysed. In the absence of IL-22, there was a response of hepcidin, resulting in a reduction in serum iron levels. However, the hypoferremic response to LPS was slightly blunted in mice lacking IL-22, suggesting that, during LPS-mediated inflammation, IL-22 may play a minor role in mediating the hypoferremic response. These results may have implications for the treatment and management of the ACD. |
