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支气管肺发育不良中类胰蛋白酶免疫反应性肥大细胞增生

Tryptase immunoreactive mast cell hyperplasia in bronchopulmonary dysplasia.

作者信息

Lyle R E, Tryka A F, Griffin W S, Taylor B J

机构信息

Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, USA.

出版信息

Pediatr Pulmonol. 1995 Jun;19(6):336-43. doi: 10.1002/ppul.1950190605.

DOI:10.1002/ppul.1950190605
PMID:7567212
Abstract

Bronchopulmonary dysplasia (BPD), the most common cause of chronic lung disease in prematurely born infants, is histologically characterized by various degrees of airway and alveolar septal fibrosis. Tryptase, a serine protease specific to mast cells, has been shown to have potent fibroblast mitogenic properties and in addition has been shown to be increased in adult fibrotic lung disorders. Based on this analogy, the distribution of pulmonary mast cells exhibiting tryptase immunoreactivity was investigated by immunoperoxidase staining in autopsy specimens of infants dying with BPD. Morphologically normal lung specimens from similarly aged infants dying of sudden infant death syndrome (SIDS) served as controls. Tryptase-positive mast cell counts were performed at 250x from at least 10 random fields in bronchial, peribronchiolar, and alveolar regions. Compared to controls, in lung sections exhibiting typical histologic features of long-standing BPD, tryptase positive cells were significantly increased in bronchial (23.9 +/- 3.6 vs 14.4 +/- 2.3) and peribronchiolar (15.3 +/- 3.2 vs 4.63 +/- 0.6) regions compared to controls (P < 0.05, Student's t test). In particular, alveolar regions exhibiting moderate to severe degrees of septal fibrosis exhibited a dramatic increase in the number of tryptase-positive cells (9.83 +/- 1.89 vs 0.34 +/- 0.18, P = 0.003). These findings of a tryptase-positive mast cell hyperplasia in BPD suggest potential roles of mast cells as well as tryptase in the pathogenesis of this disease.

摘要

支气管肺发育不良(BPD)是早产婴儿慢性肺病的最常见病因,其组织学特征为不同程度的气道和肺泡间隔纤维化。类胰蛋白酶是肥大细胞特有的一种丝氨酸蛋白酶,已被证明具有强大的成纤维细胞促有丝分裂特性,此外,在成人肺纤维化疾病中其水平也会升高。基于此相似性,通过免疫过氧化物酶染色,对死于BPD的婴儿尸检标本中表现出类胰蛋白酶免疫反应性的肺肥大细胞分布进行了研究。死于婴儿猝死综合征(SIDS)的同龄婴儿的形态学正常肺标本作为对照。在支气管、支气管周围和肺泡区域至少10个随机视野中,以250倍放大倍数进行类胰蛋白酶阳性肥大细胞计数。与对照组相比,在表现出长期BPD典型组织学特征的肺切片中,支气管(23.9±3.6对14.4±2.3)和支气管周围(15.3±3.2对4.63±0.6)区域的类胰蛋白酶阳性细胞显著增加(P<0.05,学生t检验)。特别是,表现出中度至重度间隔纤维化的肺泡区域,类胰蛋白酶阳性细胞数量显著增加(9.83±1.89对0.34±0.18,P = 0.003)。BPD中类胰蛋白酶阳性肥大细胞增生的这些发现表明肥大细胞以及类胰蛋白酶在该疾病发病机制中可能发挥的作用。

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