Interleukin-3 amplifies acute inflammation and is a potential therapeutic target in sepsis

Georg F. Weber, Benjamin G. Chousterman, Shun He, Ashley M. Fenn, Manfred Nairz, Atsushi Anzai, Thorsten Brenner, Florian Uhle, Yoshiko Iwamoto, Clinton S. Robbins, Lorette Noiret, Sarah L. Maier, Tina Zönnchen, Nuh N. Rahbari, Sebastian Schölch, Anne Klotzsche Von Ameln, Triantafyllos Chavakis, Jürgen Weitz, Stefan Hofer, Markus A. WeigandMatthias Nahrendorf, Ralph Weissleder, Filip K. Swirski

研究成果: Article査読

257 被引用数 (Scopus)


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-6Chigh 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.

出版ステータスPublished - 2015 3月 13

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