Cutting Edge: IL-1α and Not IL-1β Drives IL-1R1-Dependent Neonatal Murine Sepsis Lethality.

Benjamin JT, Moore DJ, Bennett C, van der Meer R, Royce A, Loveland R, Wynn JL
J Immunol. 2018 201 (10): 2873-2878

PMID: 30305325 · PMCID: PMC6219910 · DOI:10.4049/jimmunol.1801089

Sepsis disproportionately affects the very old and the very young. IL-1 signaling is important in innate host defense but may also play a deleterious role in acute inflammatory conditions (including sepsis) by promulgating life-threatening inflammation. IL-1 signaling is mediated by two distinct ligands: IL-1α and IL-1β, both acting on a common receptor (IL-1R1). IL-1R1 targeting has not reduced adult human sepsis mortality despite biologic plausibility. Because the specific role of IL-1α or IL-1β in sepsis survival is unknown in any age group and the role of IL-1 signaling remains unknown in neonates, we studied the role of IL-1 signaling, including the impact of IL-1α and IL-1β, on neonatal murine sepsis survival. IL-1 signaling augments the late plasma inflammatory response to sepsis. IL-1α and not IL-1β is the critical mediator of sepsis mortality, likely because of paracrine actions within the tissue. These data do not support targeting IL-1 signaling in neonates.

Copyright © 2018 by The American Association of Immunologists, Inc.

MeSH Terms (14)

Animals Animals, Newborn Female Humans Infant, Newborn Inflammation Interleukin-1alpha Interleukin-1beta Male Mice Mice, Inbred C57BL Receptors, Interleukin-1 Type I Sepsis Signal Transduction

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