Figure 1. The host response to sepsis. The host response to sepsis is characterized by both pro-inflammatory responses and anti-inflammatory immune suppressive responses. Inflammatory responses are initiated by interaction between pathogen-associated molecular patterns (PAMPs) expressed by pathogens or endogenous danger signals (danger-associated molecular patterns, DAMPs) and pattern recognition receptors (PRR) expressed by host immune cells. Exaggerated inflammation with collateral tissue damage and necrotic cell death will result in the release of DAMPs that can perpetuate ongoing inflammation. The pro-inflammatory response is enhanced by activation of leukocytes, complement, and the coagulation system. The anti-inflammatory immune suppressive response depends on impaired function of immune cells, neuroendocrine regulation, and inhibition of pro-inflammatory gene transcription. Importantly, direction, extent, and duration of the septic response is determined by both host factors, such as genetic composition, age, comorbidity, and medication, and pathogen factors, including microbial load and virulence. LPS, lipopolysaccharide; LTA, lipoteichoic acid; HSP, heat shock protein; HMGB-1, high mobility group box-1 protein; IL, interleukin; IL-1RA, IL-1 receptor antagonist; MRP8/14, migration inhibitory factor-related protein-8/14; NETs, neutrophils extracellular traps; T, T lymphocytes; B, B lymphocytes; DC, dendritic cells; Tregs, regulatory T lymphocytes; TLR, toll-like receptor.