Immunity in sepsis

Abstract

Sepsis, now defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, initiates a complex interplay of host processes. Several lines of clinical evidence show that patients with severe sepsis not only exhibited an exaggerated inflammation but also exhibited multiple defects in adaptive immunity. Data suggest that a subgroup of septic patients with severe immune alterations is at high risk of death or nosocomial infection and therefore could benefit from adjunctive immune stimulating therapies. This finding has been termed the persistent inflammation/immunosuppression and catabolism syndrome. The immediate inflammatory response is presumed to be predominantly driven by danger signals produced by pathogens, which bind to innate immune receptors activating a complex intracellular signaling system that leads to the expression of several common gene classes that are involved in inflammation, adaptive immunity, and cellular metabolism, but pathophysiology of immunosuppression is not completely understood. This review details the mediators in sepsis linking to innate and adaptive immune systems to explain part of pathophysiology of this severe condition.