Leprosy: contribution of mast cells to epineurial collagenization.
Leprosy: contribution of mast cells to epineurial collagenization.
复制标题
麻风病：肥大细胞对神经外膜胶原化的贡献。
作者：
N. Montagna;M. L. D. De Oliveira;C. Mandarim;L. Chimelli
背景
麻风病是由麻风分枝杆菌引起的一种疾病，是世界范围内的一个重要健康问题。它是造成不可逆神经损伤的原因，其中纤维化起着重要作用。肥大细胞和不同纤维化条件之间的相互作用的存在早已被观察到。类胰蛋白酶是人肥大细胞中最丰富的蛋白质产物，已显示其对成纤维细胞具有促有丝分裂作用并增加I型胶原蛋白的产生。
患者和方法
为探讨类胰蛋白酶肥大细胞与麻风神经纤维化的可能关系，我们对24例麻风神经病患者的腓肠神经活检进行了研究。肥大细胞与小鼠抗人肥大细胞抗类胰蛋白酶克隆AA1染色以及纤维化，定量估计在两个epi和神经内膜隔室。
结果
麻风神经外膜中胶原蛋白增加与富含类胰蛋白酶的肥大细胞密度之间存在显着相关性，但在神经内膜中则不然。
结论
由于麻风的神经外膜富含I型胶原，本研究结果支持富含类胰蛋白酶的肥大细胞通过类胰蛋白酶分泌对麻风神经外膜胶原化的贡献。
BACKGROUND
Leprosy, a disease caused by Mycobacterium leprae, is an important health problem worldwide. It is responsible for an irreversible nerve damage in which fibrosis plays an important role. The existence of an interaction between mast cells and different fibrotic conditions has long been observed. Tryptase, the most abundant protein product of human mast cells, has been shown to be mitogenic for fibroblasts and to increase type I collagen production.
PATIENTS AND METHODS
In order to explore the possible relationship between tryptase-rich mast cells and nerve fibrosis in leprosy, we studied 24 sural nerve biopsies of patients with leprous neuropathy. Mast cells stained with mouse antihuman mast cell antitryptase clone AA1 as well as fibrosis, were quantitatively estimated in both epi- and endoneurial compartments.
RESULTS
There was a remarkable association between collagen increase and tryptase-rich mast cell density in the epineurium but not in the endoneurium of leprous nerves.
CONCLUSION
Since the epineurium in leprosy is type I collagen rich, the present findings support a tryptase-rich mast cell contribution to epineurial collagenization in leprosy through their tryptase secretion.