NEUTROPHIL-INDUCED HUMAN BRONCHIAL HYPERRESPONSIVENESS INVITRO - PHARMACOLOGICAL MODULATION

被引：16

作者：

HUGHES, JM ^{[1
]}

MCKAY, KO ^{[1
]}

JOHNSON, PR ^{[1
]}

TRAGOULIAS, S ^{[1
]}

BLACK, JL ^{[1
]}

ARMOUR, CL ^{[1
]}

机构：

[1] UNIV SYDNEY,DEPT PHARMACOL,SYDNEY,NSW 2006,AUSTRALIA

来源：

CLINICAL AND EXPERIMENTAL ALLERGY | 1993年 / 23卷 / 04期

关键词：

D O I：

10.1111/j.1365-2222.1993.tb00318.x

中图分类号：

R392 [医学免疫学];

学科分类号：

100102 ;

摘要：

Although it has been postulated that inflammatory cells cause the bronchial hyperresponsiveness which is diagnostic of asthma [1], until recently there has been little direct evidence of such a link. We have recently shown that calcium ionophore-activated human neutrophils and eosinophils can induce a state of human airway hyperresponsiveness in vitro [2]. In this study we have shown that the anti-inflammatory agent nedocromil sodium, 10(-7) M, inhibited the hyperresponsiveness induced by products released from ionophore activated neutrophils but did not inhibit the release of leukotriene B4 from the same cells. Neutrophil-induced bronchial hyperresponsiveness was also inhibited by pre-treatment of the bronchial tissues with a thromboxane A2 and prostaglandin receptor antagonist, GR32191, 10(-7) m. These findings indicate that cyclooxygenase products are involved in bronchial hyperresponsiveness induced by inflammatory cell products in vitro and that their release can be inhibited by nedocromil sodium.

引用

页码：251 / 256

页数：6

共 26 条

[1] CHARACTERIZATION OF CONTRACTILE PROSTANOID RECEPTORS ON HUMAN AIRWAY SMOOTH-MUSCLE [J].