Department of Theoretical Health Sciences and Health Management, Faculty of Health Sciences and Social Studies, University of Szeged, Temesvári krt. 31, Szeged, H-6726, Hungary.
HUN-REN-SZTE Neuroscience Research Group, Hungarian Research Network, Danube Neuroscience Research Laboratory, University of Szeged (HUN-REN-SZTE), Tisza Lajos krt. 113, Szeged, H- 6725, Hungary.
J Headache Pain. 2024 Aug 7;25(1):129. doi: 10.1186/s10194-024-01833-z.
Migraine, a primary headache disorder whose mechanism remains incompletely understood, appears to involve the activation of the trigeminovascular system (TS) during attacks. Research suggests that inflammatory processes mediated by the immune system may play a role in migraine pathophysiology. Neuroinflammation is often associated with migraine attacks, with cytokines serving as crucial mediators in the process. Elevated levels of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), have been observed in the blood and cerebrospinal fluid of individuals experiencing migraine attacks. These cytokines have the capacity to sensitize pain pathways in the brain, thereby increasing sensitivity to pain stimuli. This phenomenon, known as central sensitization, is believed to contribute to the intensity and persistence of migraine pain. Kynurenines, endogenous mediators of glutamatergic mechanisms, can significantly influence the pathophysiology of primary headache disorders. The kynurenine system is collectively known as the kynurenine pathway (KP), which can act on multiple receptors, such as glutamate receptors, aryl hydrocarbon receptors (AhRs), G protein-coupled receptors 35 (GPR35), and α-7 nicotinic acetylcholine (α7 nACh) receptors. These receptors are also found on various cells of the immune system, so the role of the KP in the pathomechanism of primary headaches may also be mediated through them. In this review, our goal is to show a possible link between the receptors of the KP and immune system in the context of inflammation and migraine. Migraine research in recent years has focused on neuropeptides, such as calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide (PACAP) as potential pathogenic factors and possible therapeutic approaches. These peptides share many similarities in their characteristics and roles. For instance, they exhibit potent vasodilation, occur in both the peripheral and central nervous systems, and play a role in transmitting nociception and neurogenic inflammation. The investigation of potential connections between the aforementioned neuropeptides and the kynurenine pathway could play a significant role in uncovering the pathomechanism of migraine and identifying new drug candidates.
偏头痛是一种原发性头痛障碍,其发病机制尚不完全清楚,在发作期间似乎涉及三叉神经血管系统 (TS) 的激活。研究表明,免疫系统介导的炎症过程可能在偏头痛病理生理学中发挥作用。神经炎症常与偏头痛发作有关,细胞因子在该过程中起着关键的介质作用。在经历偏头痛发作的个体的血液和脑脊液中,观察到促炎细胞因子(如白细胞介素-1β (IL-1β)、白细胞介素-6 (IL-6) 和肿瘤坏死因子-α (TNF-α))水平升高。这些细胞因子能够使大脑中的疼痛通路敏感化,从而增加对疼痛刺激的敏感性。这种现象称为中枢敏化,被认为是偏头痛疼痛强度和持续时间的原因。色氨酸代谢产物是谷氨酸能机制的内源性介质,可显著影响原发性头痛障碍的病理生理学。色氨酸代谢产物系统统称为色氨酸途径 (KP),可作用于多种受体,如谷氨酸受体、芳基烃受体 (AhR)、G 蛋白偶联受体 35 (GPR35) 和 α-7 烟碱乙酰胆碱 (α7 nACh) 受体。这些受体也存在于免疫系统的各种细胞上,因此 KP 在原发性头痛的发病机制中的作用也可能通过它们介导。在这篇综述中,我们的目标是展示 KP 的受体与免疫系统在炎症和偏头痛背景下的可能联系。近年来,偏头痛研究的重点是神经肽,如降钙素基因相关肽 (CGRP) 和垂体腺苷酸环化酶激活肽 (PACAP),作为潜在的致病因素和可能的治疗方法。这些肽在其特征和作用方面有许多相似之处。例如,它们表现出强烈的血管扩张作用,存在于外周和中枢神经系统中,在传递伤害感受和神经源性炎症方面发挥作用。研究上述神经肽与色氨酸途径之间的潜在联系可能对揭示偏头痛的发病机制和确定新的候选药物具有重要意义。