Hartmannsberger Beate, Ben-Kraiem Adel, Kramer Sofia, Guidolin Carolina, Kazerani Ida, Doppler Kathrin, Thomas Dominique, Gurke Robert, Sisignano Marco, Kalelkar Pranav P, García Andrés J, Monje Paula V, Sammeth Michael, Nusrat Asma, Brack Alexander, Krug Susanne M, Sommer Claudia, Rittner Heike L
Centre for Interdisciplinary Pain Medicine, Department of Anaesthesiology, Intensive Care, Emergency and Pain Medicine, University Hospital Würzburg, Würzburg, Germany.
Helmholtz Institute for Metabolic, Obesity and Vascular Research, Diet-Induced Metabolic Alterations Group, Leipzig, Germany.
Acta Neuropathol. 2024 Dec 16;149(1):1. doi: 10.1007/s00401-024-02840-9.
Nerve injury causes neuropathic pain and multilevel nerve barrier disruption. Nerve barriers consist of perineurial, endothelial and myelin barriers. So far, it is unclear whether resealing nerve barriers fosters pain resolution and recovery. To this end, we analysed the nerve barrier property portfolio, pain behaviour battery and lipidomics for precursors of specialized pro-resolving meditators (SPMs) and their receptors in chronic constriction injury of the rat sciatic nerve to identify targets for pain resolution by resealing the selected nerve barriers. Of the three nerve barriers-perineurium, capillaries and myelin-only capillary tightness specifically against larger molecules, such as fibrinogen, recuperated with pain resolution. Fibrinogen immunoreactivity was elevated in rats not only at the time of neuropathic pain but also in nerve biopsies from patients with (but not without) painful polyneuropathy, indicating that sealing of the vascular barrier might be a novel approach in pain treatment. Hydroxyeicosatetraenoic acid (15R-HETE), a precursor of aspirin-triggered lipoxin A4, was specifically upregulated at the beginning of pain resolution. Repeated local application of resolvin D1-laden nanoparticles or Fpr2 agonists sex-independently resulted in accelerated pain resolution and fibrinogen removal. Clearing macrophages (Cd206) were boosted and fibrinolytic pathways (Plat) were induced, while inflammation (Tnfα) and inflammasomes (Nlrp3) were unaffected by this treatment. Blocking TAM receptors (Tyro3, Axl and Mer) and tyrosine kinase receptors linking haemostasis and inflammation completely inhibited all the effects. In summary, nanoparticles can be used as transporters for fleeting lipids, such as SPMs, and therefore expand the array of possible therapeutic agents. Thus, the Fpr2-Cd206-TAM receptor axis may be a suitable target for strengthening the capillary barrier, removing endoneurial fibrinogen and boosting pain resolution in patients with chronic neuropathic pain.
神经损伤会导致神经性疼痛和多级神经屏障破坏。神经屏障由神经束膜、内皮和髓鞘屏障组成。到目前为止,尚不清楚重新封闭神经屏障是否有助于疼痛缓解和恢复。为此,我们分析了大鼠坐骨神经慢性压迫损伤中专门的促解决介质(SPM)及其受体的前体的神经屏障特性组合、疼痛行为组和脂质组学,以确定通过重新封闭选定的神经屏障来缓解疼痛的靶点。在三种神经屏障(神经束膜、毛细血管和髓鞘)中,只有毛细血管对大分子(如纤维蛋白原)的紧密性随疼痛缓解而恢复。纤维蛋白原免疫反应性不仅在神经性疼痛时在大鼠中升高,而且在患有(而非未患有)疼痛性多发性神经病患者的神经活检中也升高,这表明封闭血管屏障可能是疼痛治疗的一种新方法。羟基二十碳四烯酸(15R-HETE),一种阿司匹林触发的脂氧素A4的前体,在疼痛缓解开始时特异性上调。反复局部应用载有消退素D1的纳米颗粒或Fpr2激动剂可性别独立地加速疼痛缓解和纤维蛋白原清除。清除性巨噬细胞(Cd206)增加,纤维蛋白溶解途径(Plat)被诱导,而炎症(Tnfα)和炎性小体(Nlrp3)不受该治疗影响。阻断TAM受体(Tyro3、Axl和Mer)以及连接止血和炎症的酪氨酸激酶受体完全抑制了所有这些作用。总之,纳米颗粒可作为短暂性脂质(如SPM)的转运体,从而扩大了可能的治疗药物范围。因此,Fpr2-Cd206-TAM受体轴可能是加强毛细血管屏障、清除神经内膜纤维蛋白原和促进慢性神经性疼痛患者疼痛缓解的合适靶点。