囊性纤维化患者多形核白细胞对白三烯B4的趋化反应降低。
Decreased polymorphonuclear leucocyte chemotactic response to leukotriene B4 in cystic fibrosis.
作者信息
Lawrence R H, Sorrelli T C
机构信息
Centre for Infectious Diseases and Microbiology, Westmead Hospital, NSW, Australia.
出版信息
Clin Exp Immunol. 1992 Aug;89(2):321-4. doi: 10.1111/j.1365-2249.1992.tb06953.x.
Evidence that leukotriene B4 (LTB4) is a significant inflammatory mediator in chronic pseudomonal respiratory disease was sought in adolescents and young adults with cystic fibrosis. Specific chemotaxis of peripheral blood polymorphonuclear leucocytes (PMN) was used as an indirect measure of remote in vivo exposure to LTB4. PMN from 17 patients showed a significant decrease in chemotaxis to 10(-7)-10(-9) M LTB4, but normal responses to 10(-8) M n-formyl-methionyl-leucyl-phenylalanine and 4 mg/ml casein, when compared with 17 healthy age- and sex-matched controls. This result is consistent with chronic production of LTB4, and specific deactivation of circulating PMN receptors for LTB4 in patients with cystic fibrosis. Pharmacologic inhibition of LTB4 production in vivo may help elucidate its role in the pathogenesis of lung damage in cystic fibrosis.
在患有囊性纤维化的青少年和年轻成年人中寻找白三烯B4（LTB4）是慢性铜绿假单胞菌呼吸道疾病中重要炎症介质的证据。外周血多形核白细胞（PMN）的特异性趋化作用被用作间接衡量体内远距离暴露于LTB4的指标。与17名年龄和性别匹配的健康对照相比，17名患者的PMN对10(-7)-10(-9)M LTB4的趋化作用显著降低，但对10(-8)M N-甲酰甲硫氨酰亮氨酰苯丙氨酸和4mg/ml酪蛋白的反应正常。该结果与LTB4的慢性产生以及囊性纤维化患者循环PMN中LTB4受体的特异性失活一致。体内对LTB4产生的药理抑制可能有助于阐明其在囊性纤维化肺损伤发病机制中的作用。
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