Pre–B cell colony–enhancing factor inhibits neutrophil apoptosis in experimental inflammation and clinical sepsis
J. Clin. Invest. Song Hui Jia, et al. 113:1318 doi:10.1172/JCI19930 [
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Figure 2Prevention of PBEF translation with an antisense oligonucleotide blocks inhibition of apoptosis in response to inflammatory stimuli. (
A) Neutrophil apoptosis, assessed as the nuclear uptake of propidium iodide, was significantly inhibited by coincubation with LPS (1 ∝g/ml), IL-1β (100 pg/ml), GM-CSF (20 ng/ml), IL-8 (250 ng/ml), or TNF-α (40 ng/ml). *
P < 0.05 compared with control rates. Prevention of PBEF translation using an antisense oligonucleotide prevented this inhibitory effect; the corresponding sense or scrambled nonsense controls were without effect. Data are mean ± SD of six separate studies. (
B) Antisense treatment of resting or LPS-stimulated (1 ∝g/ml) neutrophils inhibited the translation of PBEF as detected by Western blot analysis. Blot is representative of three separate studies. (
C) Both LPS (1 ∝g/ml) and recombinant PBEF (50 ng/ml) inhibited phosphatidylserine exteriorization detected by the binding of FITC-labeled annexin V, an effect that was specifically blocked when neutrophils were pretreated with PBEF antisense;
n = 4, *
P < 0.05. rPBEF, recombinant PBEF.