Abstract
Surgical injury can be a life‐threatening complication, not only due to the injury itself, but also due to immune responses to the injury and subsequent development of infections, which readily result in sepsis. Sepsis remains the leading cause of death in most intensive care units. Unfavorable outcomes of several high‐profile trials in the treatment of sepsis have led researchers to state that sepsis studies need a new direction. The immune response that occurs during sepsis is characterized by a cytokine‐mediated hyper‐inflammatory phase, which most patients survive, and a subsequent immunosuppressive phase. Therefore, therapies that improve host immunity might increase the survival of patients with sepsis. Many mechanisms are responsible for sepsis‐induced immunosuppression, including apoptosis of immune cells, increased regulatory T cells and expression of programmed cell death 1 on CD4+ T cells, and cellular exhaustion. Immunomodulatory molecules that were recently identified include interleukin‐7, interleukin‐15, and anti‐programmed cell death 1. Recent studies suggest that immunoadjuvant therapy is the next major advance in sepsis treatment.
Highlights
Surgical injury can be a life‐threatening complication, due to the injury itself, and due to immune responses to the injury and the subsequent development of infections with or without associated organ dysfunction
Two major consequences of endotoxin tolerance on monocytes are an increase in the release of immunosuppressive mediators, such as IL‐10, and a decrease in antigen presentation as a result of the reduced expression of human leukocyte antigen (HLA)‐DR; both are associated with a worse outcome of sepsis.[20,21]
We previously reported that expression of the human leukocyte antigen HLA‐DR by peripheral blood monocytes was decreased in septic patients, in patients with septic shock or severe sepsis.[26]
Summary
Surgical injury can be a life‐threatening complication, due to the injury itself, and due to immune responses to the injury and the subsequent development of infections with or without associated organ dysfunction. Recent studies show that the activation of both proinflammatory and anti‐inflammatory immune responses occurs promptly after the onset of sepsis.[10] Cells of the innate immune system, including monocytes and neutrophils, release high levels of proinflammatory cytokines.
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