{"title":"Anti-inflammatory and nitric oxide-inhibiting properties of granulocyte colony-stimulating factor.","authors":"G Hoffmann, W Schobersberger","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":"20 8","pages":"673-81"},"PeriodicalIF":0.0000,"publicationDate":"1999-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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.