Regulation of neutrophil apoptosis by sodium butyrate.
Neutrophils have a very short half life because they constitutively undergo apoptosis. Granulocyte-macrophage colony-stimulating factor (GM-CSF) can delay apoptosis, but this agent also primes functions such as the respiratory burst and receptor upregulation. Here, we show that sodium butyrate, which has been shown to increase gene expression and differentiation in a variety of cell types, is more effective than GM-CSF in delaying neutrophil apoptosis. Thus, sodium butyrate preserves cell morphology and function, and butyrate-treated cells express high levels of CD16 after overnight culture. However, neither GM-CSF nor sodium butyrate appear to affect mRNA levels for CD16.
Moulding
D
D
Department of Biochemistry, University of Liverpool, U.K.
Quayle
J A
JA
Stringer
R E
RE
Hart
C A
CA
Edwards
S W
SW
D017209:Apoptosis / Q000187:drug effects*; D002087:Butyrates / Q000494:pharmacology*; D020148:Butyric Acid; D003513:Cycloheximide / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D017452:Receptors, IgG / Q000096:biosynthesis / Q000235:genetics
D002087:Butyrates; D007375:Interleukin-1; D017452:Receptors, IgG; D020148:Butyric Acid; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D003513:Cycloheximide