EOSINOPHIL CATIONIC PROTEIN STIMULATES AND MAJOR BASIC-PROTEIN INHIBITS AIRWAY MUCUS SECRETION

被引:55
作者
LUNDGREN, JD
DAVEY, RT
LUNDGREN, B
MULLOL, J
MAROM, Z
LOGUN, C
BARANIUK, J
KALINER, MA
SHELHAMER, JH
机构
[1] NIAID, CTR CLIN, DEPT CRIT CARE MED, BETHESDA, MD 20892 USA
[2] NIAID, DIV PARASITOL, BETHESDA, MD 20892 USA
[3] NIAID, ALLERG DIS SECT, BETHESDA, MD 20892 USA
[4] MT SINAI MED CTR, NEW YORK, NY 10029 USA
关键词
D O I
10.1016/0091-6749(91)90390-A
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Possible roles of eosinophil (EO) products in modulating the release of mucus from airway explants were investigated. Cell- and membrane-free lysates from purified human EOs (1 to 20 x 10(5)) caused a dose-dependent release of respiratory glycoconjugates (RGC) from cultured feline tracheal explants. Crude extracts from isolated EO granules also stimulated RGC release, suggesting that a granular protein might be responsible. Three proteins derived from EO granules, EO-derived neurotoxin, EO cationic protein (ECP), and major basic protein (MBP) were separated by sequential sizing and affinity chromatography. ECP (0.025 to 25-mu-g/ml) caused a dose-dependent increase in RGC release from both feline and human airway explants and also stimulated the release of the serous cell-marker, lactoferrin, from human bronchial explants. EO-derived neurotoxin (0.025 to 50-mu-g/ml) failed to affect RGC release, whereas MBP (50-mu-g/ml) significantly inhibited RGC release from feline explants. Thus, ECP stimulates RGC and lactoferrin release from airway explants, whereas MBP inhibits RGC release.
引用
收藏
页码:689 / 698
页数:10
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