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Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Science 2015 ; 347 (6227): 1260-5 Nephropedia Template TP
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Interleukin-3 amplifies acute inflammation and is a potential therapeutic target in sepsis #MMPMID25766237
Weber GF; Chousterman BG; He S; Fenn AM; Nairz M; Anzai A; Brenner T; Uhle F; Iwamoto Y; Robbins CS; Noiret L; Maier SL; Zonnchen T; Rahbari NN; Scholch S; Klotzsche-von Ameln A; Chavakis T; Weitz J; Hofer S; Weigand MA; Nahrendorf M; Weissleder R; Swirski FK
Science 2015[Mar]; 347 (6227): 1260-5 PMID25766237show ga
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.