Authors: Lee CR, Zeldin DC

PMID: 26605933 PMCID: PMC5512422 doi: 10.1056/NEJMcibr1511280


Severe sepsis remains a major public health problem associated with poor clinical outcomes and substantial health care expenditures. Although the number of sepsis cases in the United States exceeds 750,000 per year and sepsis is associated with an estimated mortality rate of 20–30%, there is a lack of effective treatments.1 There is also an urgent need to develop new therapeutic strategies due to the rise of antibiotic resistant bacteria.2 Therapies that inhibit the activation phase of the acute inflammatory response to infection (e.g., corticosteroids, NSAIDs, anti-TNFα) have repeatedly failed to improve patient outcomes in severe sepsis. In contrast, strategies that promote endogenous factors that actively resolve the acute inflammatory response have not been rigorously explored since the key mediators that regulate this process have remained enigmatic. In this regard, Dalli and colleagues3 discovered a new group of host protective lipids termed 13-series resolvins (RvTs) that are formed during the very early phase of inflammation, promote bacterial phagocytosis, and augment host recovery from systemic infection by accelerating resolution of the acute inflammatory response.

Keywords: sepsis, infectious inflammation