Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany.
Clin Exp Allergy. 2011 Oct;41(10):1392-9. doi: 10.1111/j.1365-2222.2011.03795.x. Epub 2011 Jun 16.
Chronic spontaneous urticaria is triggered by many direct and indirect aggravating factors including autoreactive/autoimmune mechanisms, infections, non-allergic and pseudoallergic intolerance reactions. However, the role of neuroimmune mechanisms in chronic spontaneous urticaria so far is unclear.
Thus, we wanted to address the regulation of the neurotrophin brain-derived neurotrophic factor (BDNF) in serum and inflammatory skin of patients with chronic spontaneous urticaria in comparison to subjects with healthy skin.
Fifty adult patients with chronic spontaneous urticaria and 23 skin-healthy subjects were studied. Chronic spontaneous urticaria was defined as recurrent weals for more than 6 weeks. Autologous serum skin test was performed in all patients with chronic spontaneous urticaria and BDNF serum levels were analysed by enzyme immunoassay in all subjects. Furthermore, skin biopsies were taken from weals of eight patients with chronic spontaneous urticaria as well as from healthy skin of eight controls to evaluate the expression of BDNF and its receptors including tyrosine kinase (trk) B and pan-neurotrophin receptor p75(NTR) by immunohistochemistry.
BDNF serum levels were detectable in all subjects studied. However, BDNF levels were significantly higher in patients with chronic spontaneous urticaria compared to non-atopic skin-healthy controls (P<0.001). Furthermore, epidermal and dermal expression of BDNF and epidermal expression of p75(NTR) was significantly higher in patients with chronic spontaneous urticaria compared with controls (P<0.05-0.001). There was no difference with regard to the expression of trkB between chronic spontaneous urticaria and controls and no difference in BDNF serum levels between autologous serum skin test-positive (n=23) and -negative (n=27) patients with chronic spontaneous urticaria.
This study shows that BDNF is increased in serum and diseased skin of patients with chronic spontaneous urticaria, suggesting a role for neurotrophins in the pathophysiology of this chronic inflammatory skin disease. Further studies are needed to address the functional role of BDNF on key target effector cells in chronic spontaneous urticaria to establish new therapeutic implications.
慢性自发性荨麻疹是由许多直接和间接的加重因素引起的，包括自身反应/自身免疫机制、感染、非过敏性和假性过敏不耐受反应。然而，神经免疫机制在慢性自发性荨麻疹中的作用目前尚不清楚。
因此，我们想研究慢性自发性荨麻疹患者血清和炎症性皮肤中脑源性神经营养因子（BDNF）的调节情况，并与健康皮肤的受试者进行比较。
研究了 50 名成年慢性自发性荨麻疹患者和 23 名皮肤健康受试者。慢性自发性荨麻疹定义为反复发作的风团超过 6 周。所有慢性自发性荨麻疹患者均进行自体血清皮肤试验，所有受试者均采用酶联免疫吸附法分析 BDNF 血清水平。此外，从 8 例慢性自发性荨麻疹患者的风团和 8 例对照者的健康皮肤中采集皮肤活检组织，通过免疫组化法评估 BDNF 及其受体（包括酪氨酸激酶（trk）B 和泛神经生长因子受体 p75（NTR））的表达。
所有研究对象均能检测到 BDNF 血清水平。然而，与非特应性皮肤健康对照组相比，慢性自发性荨麻疹患者的 BDNF 水平明显升高（P<0.001）。此外，与对照组相比，慢性自发性荨麻疹患者的表皮和真皮 BDNF 表达以及表皮 p75（NTR）表达均显著升高（P<0.05-0.001）。慢性自发性荨麻疹患者与对照组 trkB 的表达无差异，自体血清皮肤试验阳性（n=23）和阴性（n=27）患者的 BDNF 血清水平亦无差异。
本研究表明，BDNF 在慢性自发性荨麻疹患者的血清和皮损中增加，提示神经营养因子在这种慢性炎症性皮肤病的病理生理过程中发挥作用。需要进一步研究以确定 BDNF 在慢性自发性荨麻疹的关键靶效应细胞中的功能作用，从而建立新的治疗意义。
