Comparison of prostaglandins E2 and D2 as inhibitors of respiratory burst in neutrophils from atopic and nonatopic subjects.
Neutrophils from atopic and nonatopic donors were treated with prostaglandins D2 and E2 before stimulation of the respiratory burst. Both agents inhibited neutrophil response to formyl-methionyl-leucyl-phenylalanine, but superoxide production was inhibited much more profoundly by D2 than by E2. Inhibition was similar in atopics and nonatopics. Phorbol myristate acetate stimulation of superoxide production was not significantly altered by prostaglandins. These findings suggest that minor alterations in pathways of prostaglandin synthesis may have major effects on modulation of neutrophil function, and exploration of the mechanism of stimulus-specific inhibition may further elucidate the role of neutrophils in the inflammatory response.
Styrt
B
B
Department of Medicine, New England Center, Boston, Massachusetts.
Klempner
M S
MS
Rocklin
R E
RE
D015232:Dinoprostone; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D006969:Hypersensitivity, Immediate / Q000378:metabolism*; D066298:In Vitro Techniques; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D010101:Oxygen Consumption; D015230:Prostaglandin D2; D011457:Prostaglandins D / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology*; D013481:Superoxides / Q000037:antagonists & inhibitors
D011457:Prostaglandins D; D011458:Prostaglandins E; D013481:Superoxides; D006861:Hydrogen Peroxide; D015232:Dinoprostone; D015230:Prostaglandin D2