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Sepsis, trauma, burns, and major surgical procedures activate common systemic inflammatory pathways. Nosocomial infection, organ failure, and mortality in this patient population are associated with a quantitatively different reprioritization of the circulating leukocyte transcriptome to the initial inflammatory insult, greater in both magnitude and duration, and secondary to multiple observed defects in innate and adaptive immune function. Dysregulation of inflammatory resolution processes and associated bioactive lipid mediators (LMs) mechanistically contribute to this phenotype. Recent data indicate the potential efficacy of therapeutic interventions that either reduce immunosuppressive prostaglandins (PGs) or increase specialized proresolving LMs. Here, we reassess the potential for pharmacological manipulation of these LMs as therapeutic approaches for the treatment of critical illness (CI).

Original publication

DOI

10.1016/j.it.2013.10.008

Type

Journal article

Journal

Trends immunol

Publication Date

01/2014

Volume

35

Pages

12 - 21

Keywords

cyclooxygenase, eicosanoids, immunosuppression, prostaglandins, resolution of inflammation, sepsis, Animals, Critical Illness, Humans, Inflammation, Inflammation Mediators, Lipid Metabolism, Signal Transduction