Inhibition of Neutrophil Apoptosis and Modulation of the Inflammatory Response by Granulocyte Colony‐Stimulating Factor in Healthy and Ethanol‐Treated Human Volunteers

Dalhoff, K; Hansen, F; Drömann, Daniel; Schaaf, Bernhard; Aries, Sven Philip; Braun, J.

doi:10.1086/515350

Cited by 34 publications

(32 citation statements)

References 14 publications

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“…We now further confirm the observations of Dalhoff et al that ethanol promotes neutrophil apoptosis [44]. It appears that ethanol-induced neutrophil apoptosis may not only decrease the availability of a required number of neutrophils but may also compromise the function of neutrophils.…”

Section: Discussionsupporting

confidence: 90%

Ethanol-induced neutrophil apoptosis is mediated through nitric oxide

Singhal

Patel²,

Nahar³

et al. 1999

Journal of Leukocyte Biology

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Clinical reports indicate that acute ethanol intoxication in chronic ethanol abusers is associated with neutropenia. We hypothesize that ethanol accelerates the apoptosis of neutrophils thus decreasing the peripheral blood count of neutrophils. We studied the effect of ethanol on neutrophil apoptosis in vivo as well as in vitro. Human neutrophils harvested from healthy subjects after an alcohol drinking binge showed enhanced apoptosis (before, 0.5 ؎ 0.25 vs. after, 26.1 ؎ 2.6% apoptotic neutrophils/field). Peritoneal neutrophils isolated from ethanol-treated rats also showed increased (P F 0.0001) apoptosis when compared with neutrophils isolated from control rats (

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Section: Discussionsupporting

confidence: 90%

Ethanol-induced neutrophil apoptosis is mediated through nitric oxide

Singhal

Patel²,

Nahar³

et al. 1999

Journal of Leukocyte Biology

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“…IFN-g and GM-CSF (Hartung et al, 1995;Dalhoff et al, 1998). These findings suggest that G-CSF may have an antiinflammatory role, rendering G-CSF a candidate for the prevention and treatment of Gram-negative infection (Lorenz et al, 1994;Lundblad et al, 1996;Villa et al, 1998).…”

mentioning

confidence: 99%

Granulocyte colony‐stimulating factor (G‐CSF) induces the production of cytokines in vivo

Höglund

Håkansson

2000

Br J Haematol

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Granulocyte colony‐stimulating factor (G‐CSF) is a haematopoietic growth factor required for the proliferation and differentiation of haematopoietic precursors of neutrophil granulocytes and is now used to overcome congenital and acquired neutropenia. In addition to increasing the numbers of neutrophils in vivo and modulating neutrophil functions, G‐CSF may induce the production of cytokines such as tumour necrosis factor α (TNF‐α). In the present study, the plasma levels of granulocyte–macrophage colony‐stimulating factor (GM‐CSF) in six healthy volunteers given G‐CSF at 10 μg/kg once daily for 6 d were measured and found to be elevated. The elevated levels (P < 0·05) were detected on day 2, peaked on days 6–7 and returned to baseline on day 12. In vitro, G‐CSF did not enhance the secretion of TNF‐α and GM‐CSF from mononuclear cells, whole blood or endothelial cells. However, in the co‐presence of whole blood and endothelial cells, the secretion of TNF‐α was significantly enhanced by G‐CSF at low concentrations. The GM‐CSF secretion, however, was unaltered. G‐CSF pretreatment of whole blood suppressed lipopolysaccharide (LPS)‐induced secretion of TNF‐α and GM‐CSF in a dose‐dependent manner. These results together with our previous findings suggest that G‐CSF induces the production of TNF‐α and GM‐CSF in vivo, and that this production may be due to the co‐effects of endothelial cells and whole blood under the influence of G‐CSF through an as yet unknown network of cells and cytokines. Treatment of whole blood with G‐CSF suppresses LPS‐induced secretion of TNF‐α and GM‐CSF.

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“…29 Recently, anti-inflammatory properties of G-CSF by downregulation of TNF-␣, IL-12, and IFN-␣ release in response to LPS after a prolonged administration of G-CSF at dosages even lower than used for stem cell mobilisation have been reported. [30][31][32] In contrast, short-term administration or single-dose G-CSF was found to increase plasma levels of TNF-␣ in healthy volunteers receiving endotoxin, 33 thereby probably augmenting inflammatory processes.…”

Section: Discussionmentioning

confidence: 94%

Unusual adverse events following peripheral blood stem cell (PBSC) mobilisation using granulocyte colony stimulating factor (G-CSF) in healthy donors

Hilbe

Nußbaumer

Bonatti

et al. 2000

Bone Marrow Transplant

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Summary:Here, we describe two cases of severe pyogenic infection in healthy donors diagnosed immediately following stem cell mobilisation with G-CSF. In the first donor a painful perianal abscess and in the second one an apical abscess required surgical incision. The reported serious adverse events in the literature are reviewed and the potential pathophysiological role of G-CSF or GM-CSF in augmenting inflammatory processes is discussed. In the light of a rapidly increasing number of related and unrelated peripheral blood stem cell donations the need for more comprehensive donor work-up and follow-up for peripheral blood stem cell donors has to be considered. Bone Marrow Transplantation (2000) 26, 811-813.

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Inhibition of Neutrophil Apoptosis and Modulation of the Inflammatory Response by Granulocyte Colony‐Stimulating Factor in Healthy and Ethanol‐Treated Human Volunteers

Cited by 34 publications

References 14 publications

Ethanol-induced neutrophil apoptosis is mediated through nitric oxide

Ethanol-induced neutrophil apoptosis is mediated through nitric oxide

Granulocyte colony‐stimulating factor (G‐CSF) induces the production of cytokines in vivo

Unusual adverse events following peripheral blood stem cell (PBSC) mobilisation using granulocyte colony stimulating factor (G-CSF) in healthy donors

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