1999
DOI: 10.1097/00024382-199903000-00003
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Circulating Granulocyte Macrophage Colony-Stimulating Factor in Plasma of Patients With the Systemic Inflammatory Response Syndrome Delays Neutrophil Apoptosis Through Inhibition of Spontaneous Reactive Oxygen Species Generation

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Cited by 68 publications
(47 citation statements)
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“…It has been reported that in the settings of systemic inflammatory response syndrome, circulating GMCSF has the ability to delay neutrophil apoptosis by inhibition of the generation of reactive oxygen species. 37 Thus, the actions of GMCSF during chronic inflammation in TNFR1 À / À mice likely include promoting myelopoiesis and prolonging survival of inflammatory cells. Moreover, our current study suggests that during chronic inflammation, TNF induces GMCSF expression via TNFR2, which is counteracted by signaling via TNFR1.…”
Section: Tnfr Role In Chronic Colitismentioning
confidence: 99%
“…It has been reported that in the settings of systemic inflammatory response syndrome, circulating GMCSF has the ability to delay neutrophil apoptosis by inhibition of the generation of reactive oxygen species. 37 Thus, the actions of GMCSF during chronic inflammation in TNFR1 À / À mice likely include promoting myelopoiesis and prolonging survival of inflammatory cells. Moreover, our current study suggests that during chronic inflammation, TNF induces GMCSF expression via TNFR2, which is counteracted by signaling via TNFR1.…”
Section: Tnfr Role In Chronic Colitismentioning
confidence: 99%
“…Moreover, an imbalance between these dual immune responses, with an overwhelming release of pro-or anti-inflammatory cytokines, seems to be responsible for organ dysfunction and increased susceptibility to infections (5). Medical regulation of SIRS and CARS has been conducted to improve these adverse effects, but the most desirable means of regulation remains under investigation (6)(7)(8)(9)(10)(11).…”
Section: Introductionmentioning
confidence: 99%
“…There is some evidence that granulocyte lifespan at inflamed sites in vivo is susceptible to regulation by extrinsic signals. GM-CSF in the lavage from the lungs of patients with the adult respiratory distress syndrome (ARDS) has been shown to inhibit neutrophil apoptosis [12], and prolongation of neutrophil lifespan in vivo has been reported by circulating endogenous G-CSF [13] and GM-CSF [14]. Ligation of the Fas death receptor was also shown to induce eosinophil apoptosis in an animal model of allergic airway inflammation [15].…”
Section: Introductionmentioning
confidence: 99%