Abstract
A majority of patients with severe sepsis and septic shock survive the primary injury, but are particularly prone to develop intensive care unit-acquired infections. In addition to classical risk factors of hospital-acquired infections, some acquired immune dysfunctions may impair septic hosts’ defence. Indeed, sepsis induces quantitative and functional defects of innate and adaptive immune cells, including monocyte deactivation, defective migration of neutrophils, apoptosis of dendritic cells, impaired production of interleukin-12, apoptosis of T and B lymphocytes, and expansion of regulatory T cells, resulting in a complex post-infective immune dysfunction. Relevant animal models allowed to demonstrate the impact of sepsis on host defence towards secondary infectious insults, and provided insights into cellular and molecular mechanisms that regulate these phenomena.
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