Priming of the HL-60 cell respiratory burst response by tumor necrosis factor-alpha.
The ability of tumor necrosis factor-alpha (TNF) to prime Me2SO-differentiated HL-60 cell respiratory burst activity to N-formylmethionyleucylphenylalanine (f-Met-Leu-Phe) was determined. Cultivation of differentiated HL-60 cells with TNF induced a time- and dose-dependent increase in superoxide production following stimulation with f-Met-Leu-Phe. An increase in the respiratory burst response could be detected as early as 1 h, and was maximally enhanced at 24 h. TNF enhanced superoxide production by increasing the initial rate of production without altering the time over which HL-60 cells produced superoxide following f-Met-Leu-Phe stimulation. The dose-response to f-Met-Leu-Phe in TNF-primed cells demonstrated the same half-maximal and maximal concentrations of f-Met-Leu-Phe as seen in untreated cells. Inhibition of protein synthesis by cycloheximide prevented the primary effect of TNF. We conclude that differentiated HL-60 cells can be used to examine the mechanisms by which TNF primes the neutrophil oxidative burst response.
Klein
J B
JB
Department of Medicine, University of Louisville School of Medicine, KY.
Sonnenfeld
G
G
McLeish
K R
KR
D002454:Cell Differentiation; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007700:Kinetics; D015473:Leukemia, Promyelocytic, Acute; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D011994:Recombinant Proteins / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D009240:N-Formylmethionine Leucyl-Phenylalanine; D003513:Cycloheximide; D004121:Dimethyl Sulfoxide