Styrt B, Klempner M S, Rocklin R E
Department of Medicine, New England Center, Boston, Massachusetts.
Inflammation. 1988 Jun;12(3):213-21. doi: 10.1007/BF00920073.
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.
在刺激呼吸爆发之前,用前列腺素D2和E2处理来自特应性和非特应性供体的中性粒细胞。两种药物均抑制中性粒细胞对甲酰甲硫氨酰亮氨酰苯丙氨酸的反应,但与E2相比,D2对超氧化物产生的抑制作用更为显著。特应性和非特应性个体中的抑制作用相似。前列腺素对佛波酯刺激的超氧化物产生没有显著影响。这些发现表明,前列腺素合成途径的微小改变可能对中性粒细胞功能的调节产生重大影响,探索刺激特异性抑制的机制可能进一步阐明中性粒细胞在炎症反应中的作用。