Anti-inflammatory and nitric oxide-inhibiting properties of granulocyte colony-stimulating factor.
A proposed scheme between the possible interactions of pro- and anti-inflammatory cytokines, NO and G-CSF during severe inflammation/infection is presented. Taken together, these data indicate that G-CSF exhibits anti-inflammatory properties which may prove to be beneficial in situations associated with an increased activity of the cellular immune system. Since the suppressive effects of G-CSF on the production of pro-inflammatory mediators like TNF-alpha and nitric oxide are most likely neither cell type nor tissue specific, it is conceivable that NO release induced by pro-inflammatory mediators can be reduced by G-CSF in various organ systems and in different forms of shock. In this context, G-CSF might represent a counterregulatory mechanism directed against a downstream oriented inflammatory response to infection. Therefore, the investigation of G-CSF in the prophylaxis of nonneutropenic infections, sepsis, and other severe inflammatory disorders seems reasonable.
Hoffmann
G
G
Department of Physiology I, University of Bonn, Germany.
Schobersberger
W
W
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D006801:Humans; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II; D018805:Sepsis / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor; D009569:Nitric Oxide; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II