Prostaglandins affect the respiratory burst of human neutrophils.
The effects of prostaglandins on superoxide generation by neutrophils were investigated, since these arachidonic acid metabolites are both involved in the early phase of the inflammatory process and during later stages of neutrophil function. Preincubation of these cells for five minutes with concentrations of PGE2 ranging from 10(-7) to 10(-4) M was able to significantly reduce superoxide production in PMA-stimulated neutrophils. Other pro-inflammatory PGs tested, such as PGE1, PGF1 alpha, PGF2 alpha, inhibited the respiratory burst. The PGE2-induced inhibition was compared to that exerted by staurosporine, a PKC inhibitor. The effects of the two drugs were not additive, since the combinations of PGE2 and staurosporine reduced O2- production to the same extent as staurosporine alone. Possible interferences between PKA- and PKC-mediated transduction signals are discussed.
Sottile
A
A
Institute of General Pathology, University of Messina, Medical School, Italy.
Venza
M
M
Venza
I
I
Teti
D
D
D000470:Alkaloids / Q000494:pharmacology; D002478:Cells, Cultured; D015232:Dinoprostone / Q000494:pharmacology*; D006801:Humans; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D011453:Prostaglandins / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D016897:Respiratory Burst / Q000187:drug effects*; D019311:Staurosporine; D013481:Superoxides / Q000032:analysis / Q000378:metabolism
D000470:Alkaloids; D011453:Prostaglandins; D013481:Superoxides; D011493:Protein Kinase C; D019311:Staurosporine; D015232:Dinoprostone