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Table 1 Inflammatory mediators of sepsis

From: Post-sepsis syndrome – an evolving entity that afflicts survivors of sepsis

Inflammatory mediators of sepsis
High mobility group box-1 (HMGB1) – a late mediator of the inflammatory cascade; proposed driver of neurocognitive impairment after sepsis involves high serum levels; potential target for prevention of post-sepsis syndrome (Chavan et al. 2012)
Interleukin-1 – an early mediator of sepsis; signals for the chemotaxis of leukocytes to sites of infection; causes a rise in body temperature (fever) via the thermoregulatory center in the hypothalamus (Faix 2013)
Tumor necrosis factor-α – an early mediator of sepsis; signals for the chemotaxis of leukocytes to sites of infection; causes cachexia in malignancy and maintains granulomas in tuberculosis (Faix 2013)
Interleukin-6 – a cytokine that causes fever and stimulates production of acute phase reactants (i.e. C-reactive protein, ferritin, fibrinogen, hepcidin) (Faix 2013)
Interleukin-12 – a cytokine that induces the differentiation of T-cells and activates natural killer cells (Faix 2013)
C-reactive protein – an acute phase reactant that produces complement fixation and facilitates phagocytosis; laboratory measurement used to monitor ongoing non-specific inflammation (Faix 2013)