Facer P, Mann D, Mathur R, Pandya S, Ladiwala U, Singhal B, Hongo J, Sinicropi D V, Terenghi G, Anand P
Peripheral Neuropathy Unit, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road, London, UK.
Pain. 2000 Mar;85(1-2):231-8. doi: 10.1016/s0304-3959(99)00273-0.
While sensory loss in leprosy skin is the consequence of invasion by M. leprae of Schwann cells related to unmyelinated fibres, early loss of cutaneous pain sensation, even in the presence of nerve fibres and inflammation, is a hallmark of leprosy, and requires explanation. In normal skin, nerve growth factor (NGF) is produced by basal keratinocytes, and acts via its high affinity receptor (trk A) on nociceptor nerve fibres to increase their sensitivity, particularly in inflammation. We have therefore studied NGF- and trk A-like immunoreactivity in affected skin and mirror-site clinically-unaffected skin from patients with leprosy, and compared these with non-leprosy, control skin, following quantitative sensory testing at each site. Sensory tests were within normal limits in clinically-unaffected leprosy skin, but markedly abnormal in affected skin. Sub-epidermal PGP 9.5- and trk A- positive nerve fibres were reduced only in affected leprosy skin, with fewer fibres contacting keratinocytes. However, NGF-immunoreactivity in basal keratinocytes, and intra-epidermal PGP 9.5-positive nerve fibres, were reduced in both sites compared to non-leprosy controls, as were nerve fibres positive for the sensory neurone specific sodium channel SNS/PN3, which is regulated by NGF, and may mediate inflammation-induced hypersensitivity. Keratinocyte trk A expression (which mediates an autocrine role for NGF) was increased in clinically affected and unaffected skin, suggesting a compensatory mechanism secondary to reduced NGF secretion at both sites. We conclude that decreased NGF- and SNS/PN3-immunoreactivity, and loss of intra-epidermal innervation, may be found without sensory loss on quantitative testing in clinically-unaffected skin in leprosy; this appears to be a sub-clinical change, and may explain the lack of cutaneous pain with inflammation. Sensory loss occurred with reduced sub-epidermal nerve fibres in affected skin, but these still showed trk A-staining, suggesting NGF treatment may restore pain sensation.
虽然麻风病皮肤中的感觉丧失是麻风分枝杆菌侵入与无髓纤维相关的施万细胞的结果,但即使存在神经纤维和炎症,皮肤痛觉的早期丧失也是麻风病的一个标志,需要作出解释。在正常皮肤中,神经生长因子(NGF)由基底角质形成细胞产生,并通过其在伤害性感受器神经纤维上的高亲和力受体(trk A)发挥作用,以增加其敏感性,尤其是在炎症状态下。因此,我们研究了麻风病患者受累皮肤和临床未受累的对照部位皮肤中的NGF和trk A样免疫反应性,并在每个部位进行定量感觉测试后,将这些结果与非麻风病对照皮肤进行比较。感觉测试在临床未受累的麻风病皮肤中处于正常范围,但在受累皮肤中明显异常。仅在受累的麻风病皮肤中,表皮下PGP 9.5和trk A阳性神经纤维减少,与角质形成细胞接触的纤维较少。然而,与非麻风病对照相比,两个部位的基底角质形成细胞中的NGF免疫反应性以及表皮内PGP 9.5阳性神经纤维均减少,受NGF调节且可能介导炎症诱导的超敏反应的感觉神经元特异性钠通道SNS/PN3阳性的神经纤维也是如此。角质形成细胞trk A表达(介导NGF的自分泌作用)在临床受累和未受累皮肤中均增加,提示这是两个部位NGF分泌减少后的一种代偿机制。我们得出结论,在麻风病临床未受累皮肤的定量测试中,可能发现NGF和SNS/PN3免疫反应性降低以及表皮内神经支配丧失,但无感觉丧失;这似乎是一种亚临床变化,可能解释了炎症时皮肤无痛觉的现象。受累皮肤中表皮下神经纤维减少时出现感觉丧失,但这些神经纤维仍显示trk A染色,提示NGF治疗可能恢复痛觉。