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

2015; American Association for the Advancement of Science; Volume: 347; Issue: 6227 Linguagem: Inglês

10.1126/science.aaa4268

1095-9203

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 Maier, Tina Zönnchen, Nuh N. Rahbari, Sebastian Schölch, Anne Klotzsche-von Ameln, Triantafyllos Chavakis, Jürgen Weitz, Stefan Hofer, Markus A. Weigand, Matthias Nahrendorf, Ralph Weissleder, Filip K. Świrski,

Inflammation biomarkers and pathways

A new therapeutic target for sepsis Infections can sometimes unleash powerful immune responses that careen out of control, leading to sepsis, organ failure, and death. Although antibiotics can help to quash the infection, sepsis patients also need therapies that will rein in the immune response. Weber et al. now identify one potential target, the secreted protein interleukin-3 (IL-3) (see the Perspective by Hotchkiss). In sepsis patients, higher serum concentrations of IL-3 were correlated with higher rates of mortality. In septic mice, IL-3 caused the immune system to produce large amounts of cells called monocytes and neutrophils, which secrete highly inflammatory proteins. Blocking IL-3 protected mice from sepsis-induced death. Science , this issue p. 1260 ; see also p. 1201