The innate, unspecific immune response to bacterial and fungal infection is mediated primarily by neutrophilic granulocytes. Granulocyte colony-stimulating factor (G-CSF), an endogenous hematopoietic growth factor for neutrophils produced at the site of infection, is an integral part of this natural host defense. However, neutrophilic granulocytes also play a major role in the inflammatory response, resulting in tissue damage. Therefore, the indications for colony-stimulating factors in combating infectious diseases seemed to be limited for fear of their proinflammatory activity. In contrast to these concerns, G-CSF has proven itself to be an anti-inflammatory immunomodulator. Animal, volunteer, and patient studies have all shown that G-CSF reduces inflammatory activity by inhibiting the production or activity of the main inflammatory mediators interleukin-1, tumor necrosis factor-alpha, and interferon gamma. In conclusion, the body's G-CSF-regulated emergency recruitment of neutrophils is combined with a simultaneous limitation of the harmful inflammatory reaction. This unique pharmacologic combination of improving anti-infectious defense and inhibiting inflammation, opens up a range of new indications for G-CSF in the area of nonneutropenic infections.