Increased nerve growth factor- and tyrosine kinase A-like immunoreactivities in prurigo nodularis skin an exploration of the cause of neurohyperplasia
Increased nerve growth factor- and tyrosine kinase A-like immunoreactivities in prurigo nodularis skin an exploration of the cause of neurohyperplasia
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DOI：
10.1007/s00403-001-0285-8
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发表时间：
2002-02-01
影响因子：
3
通讯作者：
Emtestam, L
中科院分区：
文献类型：
--
作者：
Johansson, O;Liang, Y;Emtestam, L
神经营养因子及其受体在皮神经发育和损伤后的重建中起重要作用。最近的发展表明，这组分子不仅发挥神经营养作用，而且还参与免疫反应和炎症。结节性痒疹是一种以神经增生和强烈瘙痒为特征的皮肤病。本研究应用免疫组织化学方法观察神经生长因子（nerve growth factor，NGF）及其受体的定位和分布，以探讨本病神经增生的原因。在正常健康志愿者和未受累皮肤中，表皮基底层或真皮中很少见到NGF免疫反应性。在结节性黑猩猩皮肤中，表皮中也几乎没有NGF免疫反应性。然而，在真皮中，大量的细胞显示出神经生长因子样免疫反应性。在健康志愿者的正常皮肤中，在表皮中仅看到酪氨酸激酶A（trkA）的弱染色，而在真皮中，根本没有看到trkA染色。然而，在结节性脊髓炎组织中，增生的神经清楚地显示trkA免疫反应性，并且似乎仅在轴突中存在染色。用NGF和p75 NGF受体双标法，在正常皮肤表皮和真皮中均呈弱阳性反应。然而，在结节性黑色素瘤的真皮中，可以看到神经生长因子和神经生长因子受体抗体的强染色。在神经生长因子免疫反应阳性细胞较多的区域，神经生长因子受体免疫反应阳性神经较密集。结果提示，结节性黑色素瘤皮肤中存在NGF的过度表达，局部浸润的炎性细胞可能是这种NGF的来源，NGF及其受体可能参与了该病的神经增生。
Neurotrophins and their receptors play an important role in cutaneous nerve development and reconstruction after injury. Recent developments indicate that this group of molecules not only exert a neurotrophic action, but are also involved in immune responses and inflammation. Prurigo nodularis is a skin disease characterized by neurohyperplasia and intense itch. In the present study, the localization and distribution of nerve growth factor (NGF) and its receptors were explored by immunohistochemical methods, with the aim of detecting the cause of the neurohyperplasia in the disease. In normal healthy volunteers and in uninvolved skin, NGF immunoreactivity was seldom seen in the basal layer of the epidermis or in the dermis. In prurigo nodularis skin, there was also very little NGF immunoreactivity in the epidermis. However, in the dermis, a huge number of cells showed an NGF-like immunoreactivity. In normal skin of healthy volunteers, only a weak staining for tyrosine kinase A (trkA) was seen in the epidermis, whereas in the dermis, there was no trkA staining seen at all. However, in the prurigo nodularis tissue, the hyperplastic nerves clearly showed trkA immunoreactivity, and it seemed that the staining was only present in the axons. By NGF and p75 NGF receptor double-labelling, both immunoreactivities showed weak staining in the epidermis and dermis of normal skin. However, in the dermis of prurigo nodularis, strong staining for both NGF and NGF receptor antibodies was seen. NGF receptor-immunoreactive nerves were more dense in areas where there were more NGF-immunoreactive cells. The results indicate that in prurigo nodularis skin, NGF is overexpressed, locally infiltrated inflammatory cells may be the source of this NGF, and NGF and its receptors may contribute to the neurohyperplasia of the disease.