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.