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10.1126/science.aaa4268

http://scihub22266oqcxt.onion/10.1126/science.aaa4268
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25766237!4376966!25766237
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suck abstract from ncbi


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pmid25766237      Science 2015 ; 347 (6227): 1260-5
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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.
  • |Animals[MESH]
  • |B-Lymphocyte Subsets/immunology[MESH]
  • |Cytokines/immunology/metabolism[MESH]
  • |Disease Models, Animal[MESH]
  • |Humans[MESH]
  • |Inflammation[MESH]
  • |Interleukin-3/blood/*immunology/metabolism[MESH]
  • |Lipopolysaccharides/immunology[MESH]
  • |Lymphoid Tissue/immunology[MESH]
  • |Mice[MESH]
  • |Mice, Inbred BALB C[MESH]
  • |Monocytes/immunology[MESH]
  • |Myelopoiesis[MESH]
  • |Neutrophils/immunology[MESH]
  • |Peritonitis/immunology/pathology[MESH]
  • |Prognosis[MESH]


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