Disease relevance of G-CSF

• Applications of either rG-CSF or G-CSF gene transfected cells into mice give rise to leukocytosis, which can be measured easily [1].
• G-CSF-treated animals showed attenuated responses in peripheral leukopenia, excess lung water, and albumin leakage in comparison with the endotoxin-alone group [2].
• Mice with elastase-induced emphysema were treated with ATRA, granulocyte colony-stimulating factor (G-CSF), or a combination of both [3].
• Granulocyte colony-stimulating factor (G-CSF) has been used to augment both the neutrophil number and function, and its prophylactic administration has proved beneficial in animal models of sepsis [4].
• Effects of G-CSF on cardiac remodeling after acute myocardial infarction in swine [5].

High impact information on G-CSF

• Granulocyte colony-stimulating factor exacerbates acute lung injury induced by intratracheal endotoxin in guinea pigs [6].
• Lipopolysaccharide and granulocyte colony-stimulating factor delay neutrophil apoptosis and ingestion by guinea pig macrophages [7].
• Granulocyte colony-stimulating factor (G-CSF) is a cytokine that stimulates the proliferation and differentiation of hematopoietic progenitor cells committed to the neutrophil/granulocyte lineage [1].
• Cloning and sequence analysis of the immediate promoter region and cDNA of porcine granulocyte colony-stimulating factor [1].
• Resuscitated swine had elevated G-CSF and TNF-alpha gene transcription, but LR and NS groups were not different from each other (P= 0.96 and 0.10, respectively) [8].

Chemical compound and disease context of G-CSF

• Administration of G-CSF to non-neutropenic animals has been shown to improve survival in experimental models of infection, but PMNs have been implicated as mediators of acute lung injury induced by lipopolysaccharide (LPS) or bacteremia [9].

Biological context of G-CSF

• We hypothesized that, after penetrating abdominal trauma, the ideal resuscitation strategy would involve early, short-lived suppression of PMN activation to minimize secondary lung injury, followed by later enhancement of PMN chemotaxis and phagocytosis [using granulocyte colony-stimulating factor (G-CSF)] to lessen late septic complications [10].
• The effects of granulocyte colony stimulation factor (G-CSF) at concentrations of 0.08, 0.8 and 8 microg/ml on reactive oxygen species (ROS) generation and lipid peroxidation induced by cisplatin in pig blood platelets were investigated [11].
• G-CSF did not increase lung MPO, BAL cell count, or BAL protein [12].
• This study demonstrates that G-CSF has a protective effect against the oxidative stress in blood platelets caused by cisplatin [11].

Anatomical context of G-CSF

• Ultrafiltered pig leukocyte extract (UPLE, IMUNOR) potentiates hematopoiesis-stimulating effects of G-CSF in vitro and improves the outcome of treatment of hematopoietic radiation damage in mice with G-CSF [13].
• The purpose of this study was to determine actions of G-CSF on PMN function in the peritoneum [14].
• In the ischemic region, the number of apoptotic endothelial cells was smaller and the number of vessels was larger in the G-CSF treatment group than in control group [5].
• CONCLUSIONS: G-CSF in resuscitation fluids improved localization of an intra-abdominal septic focus by increased production of circulating PMNs, increased PMN extravasation into the peritoneal cavity, and increased PMN cytotoxicity at the abdominal septic focus, without exaggerating PMN-dependent reperfusion injury in the lung [14].
• The role of G-CSF and IL-6 in the granulopoiesis-stimulating activity of murine blood serum induced by perorally administered ultrafiltered pig leukocyte extract, IMUNOR(R) [15].

Associations of G-CSF with chemical compounds

• These acute changes were not exacerbated by G-CSF, but were reversed by combined AICAR + G-CSF, which implicates a physiologic role for adenosine [10].
• The results showed that G-CSF had a protective effect against cisplatin action on platelets [16].
• Variables altered by G-CSF, though not significantly, showed GO2B potential increased by 50%, lipopolysaccharide-tumor necrosis factor decreased by 50%, and improved survival versus placebo (100% vs. 70%) [12].
• In the presence of G-CSF (0.8 microg/ml) in incubation medium the inhibitory effect of cisplatin on platelet arachidonate pathway was reduced [16].
• Effects of granulocyte colony-stimulating factor on hyperoxia-induced lung injury in newborn piglets [17].

Regulatory relationships of G-CSF

• In conclusion, pretreatment with G-CSF tended to attenuate rather than enhance neutrophil-dependent acute lung responses to endotoxin [2].
• Moreover, vascular endothelial growth factor was more abundantly expressed and Akt was more strongly activated in the ischemic region of the G-CSF treatment group than of control group [5].

Other interactions of G-CSF

• Cytokine analysis showed increased IL-6, G-CSF, and TNF-alpha gene transcription in resuscitated swine compared with NF swine [18].

Analytical, diagnostic and therapeutic context of G-CSF

• Therefore these data further support the idea that G-CSF in resuscitation fluids might reduce septic complications in the multiply injured trauma patient [14].
• G-CSF has not been shown to potentiate PMN mediated pulmonary reperfusion injury [10].
• G-CSF (10 microg/kg/day, once a day) was injected subcutaneously from 24h after ligation for 7 days [5].
• Quantitative reverse transcriptase-polymerase chain reaction was used to assess granulocyte colony-stimulating factor (G-CSF), IL-6, and tumor necrosis factor-alpha (TNFalpha) messenger ribonucleic acid (mRNA) levels [19].
• Stress echocardiography revealed that G-CSF ameliorated the regional contractility of chronic myocardial ischemia [20].

References