Journal
SCIENCE
Volume 347, Issue 6227, Pages 1260-1265Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaa4268
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Funding
- NIH [5R01HL095612, R56-AI104695]
- Massachusetts General Hospital Howard M. Goodman Fellowship
- German Research Foundation [WE4892/1-2, WE4892/3-1]
- Societe Francaise d'Anesthesie-Reanimation (SFAR)
- Institut Servier
- Fondation Groupe Pasteur Mutualite
- Fulbright Scholarships (Monahan Foundation)
- Fulbright Scholarships (Harvard French Scholarship Fund)
- Erwin Schrodinger Fellowship of the Austrian Science Fund FWF [J3486-B13]
- Austrian Science Fund (FWF) [J 3486] Funding Source: researchfish
- Austrian Science Fund (FWF) [J3486] Funding Source: Austrian Science Fund (FWF)
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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.
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