The main pathways of the inflammatory circuits during SIRS and sepsis are summarized. Exogenous G-CSF (dashed lines) can interrupt a fulminant proinflammatory and anti-inflammatory response by downmodulating the action of proinflammatory TNF- and IL-1, by increasing IL-1ra (and soluble TNFR) secretion, by decreasing IL-8, by improving IL-6 consumption via IL6R (p80), by upregulating HO-1, by improving LPS clearance, and by modulating the incidence of apoptotic hematopoietic cells.