Effect of rh-GMCSF and rh-GCSF on Oxygen Free Radical Production by Human Neutrophils and Blood Monocyte-Derived Human Macrophages

Al-Shammary, Fahad J.; Al-Zamel, Faten; El-Shewemi, S.; Soliman, Rafik

doi:10.1159/000173928

Cited by 2 publications

(1 citation statement)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have shown that endotoxin exposure increases G-CSF release by pulmonary cell populations, including alveolar macrophages, fibroblasts, monocytes, and endothelial cells (52)(53)(54)(55). G-CSF levels are elevated in bronchoalveolar lavage specimens from patients with acute lung injury and contribute to reductions in neutrophil apoptosis in this setting (2,3).…”

Section: Discussionmentioning

confidence: 99%

Role of NF-κB in Endotoxemia-Induced Alterations of Lung Neutrophil Apoptosis

Kupfner

Arcaroli

Yum

et al. 2001

The Journal of Immunology

View full text Add to dashboard Cite

Acute lung injury is frequently associated with endotoxemia and is characterized by the accumulation in the lungs of large numbers of neutrophils activated to produce proinflammatory mediators. In the setting of acute lung injury, the percentage of apoptotic cells among lung neutrophils is decreased. The transcriptional regulatory factor NF-κB is activated in neutrophils and other pulmonary cell populations after endotoxemia and appears to play a central role in the development of the acute inflammatory process that leads to lung injury. Because NF-κB can modulate apoptosis through increasing expression of anti-apoptotic proteins, activation of NF-κB may contribute to the alterations in lung neutrophil apoptosis associated with acute lung injury. In the present experiments, endotoxemia resulted in decreased apoptosis and increased expression of anti-apoptotic mediators among lung neutrophils. Amounts of A1, A20, and Bcl-xL, anti-apoptotic proteins whose transcription is dependent on NF-κB, were increased in lung neutrophils after endotoxemia. Inhibition of nuclear translocation of NF-κB increased the percentage of apoptotic lung neutrophils after endotoxemia, but not back to the levels found in unmanipulated animals. Although inhibition of nuclear translocation of NF-κB prevented endotoxemia-induced increases in Bcl-xL, A1, and A20 in lung neutrophils, this intervention did not prevent endotoxemia-associated elevation of Mcl-1, an anti-apoptotic protein primarily under the transcriptional regulation of CREB. These results demonstrate that mechanisms independent of NF-κB activation play an important role in modulating lung neutrophil apoptosis after endotoxemia,

show abstract

Section: Discussionmentioning

confidence: 99%

Role of NF-κB in Endotoxemia-Induced Alterations of Lung Neutrophil Apoptosis

Kupfner

Arcaroli

Yum

et al. 2001

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

Unusual and severe symptomatic impairment of neutrophil function after one cycle of temozolomide in patients with malignant glioma

Hartmann

Herholz

Salzberger

et al. 2004

Annals of Hematology

View full text Add to dashboard Cite

Temozolomide, a recently approved cytotoxic agent for the treatment of malignant glioma, has shown promising results in the treatment studies published so far. However, cytopenia and related infectious complications have been reported in 2-8% of cases. Here we present three treatment-naive patients with malignant glioma experiencing cytopenia and/or infectious complications after the first cycle of temozolomide. Neutrophils obtained from each patient up to 6 weeks after the end of the temozolomide application showed normal phagocytic capacity but decreased oxygen radical production and thus impairment of microcidal activity. Our data suggest that a prolonged impairment of the immunological defense may occur in temozolomide-treated patients.

show abstract

Effect of rh-GMCSF and rh-GCSF on Oxygen Free Radical Production by Human Neutrophils and Blood Monocyte-Derived Human Macrophages

Cited by 2 publications

References 16 publications

Role of NF-κB in Endotoxemia-Induced Alterations of Lung Neutrophil Apoptosis

Role of NF-κB in Endotoxemia-Induced Alterations of Lung Neutrophil Apoptosis

Unusual and severe symptomatic impairment of neutrophil function after one cycle of temozolomide in patients with malignant glioma

Contact Info

Product

Resources

About