Hard to Remember: Long-Term Functional Defects in Myeloid Cells and Wound Repair After Sepsis.

Abstract

Sepsis is a highly heterogeneous syndrome caused by an unbalanced host response to an infection. Although exact data on the incidence and mortality of sepsis at a global level are lacking, a recent metaanalysis encompassing 27 studies from 7 high-income countries estimated the incidence rate at 437 for hospital-treated sepsis cases per 100 000 person-years.1 This was associated with an overall mortality of 17%, which rose to 26% in patients with severe sepsis.1 While sepsis mortality has decreased in recent years,2,3 absolute fatality numbers due to sepsis tended to increase due to the higher numbers of patients with sepsis.2,4 In addition to that and very importantly, an additional health care problem is caused by the long-term sequelae in patients who recovered from a sepsis episode: infectious complications, cognitive and physical impairments, or cardiovascular complications.5–8 However, despite the clinical importance of these long-term complications, very little is known about the pathophysiological and molecular mechanisms underlying them.