| First Author | Weber GF | Year | 2015 |
| Journal | Science | Volume | 347 |
| Issue | 6227 | Pages | 1260-5 |
| PubMed ID | 25766237 | Mgi Jnum | J:259312 |
| Mgi Id | MGI:6147932 | Doi | 10.1126/science.aaa4268 |
| Citation | Weber GF, et al. (2015) Interleukin-3 amplifies acute inflammation and is a potential therapeutic target in sepsis. Science 347(6227):1260-5 |
| abstractText | Sepsis is a frequently fatal condition characterized by an uncontrolled and harmful host reaction to microbial infection. Despite the prevalence and severity of sepsis, we lack a fundamental grasp of its pathophysiology. Here we report that the cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis. Using a mouse model of abdominal sepsis, we showed that innate response activator B cells produce IL-3, which induces myelopoiesis of Ly-6C(high) monocytes and neutrophils and fuels a cytokine storm. IL-3 deficiency protects mice against sepsis. In humans with sepsis, high plasma IL-3 levels are associated with high mortality even after adjusting for prognostic indicators. This study deepens our understanding of immune activation, identifies IL-3 as an orchestrator of emergency myelopoiesis, and reveals a new therapeutic target for treating sepsis. |
