PDF(Pubmed)
Abstract：
Chronic pain, a complex and debilitating condition, involves intricate interactions between central and peripheral inflammatory processes. Cytokines, specifically tumor necrosis factor (TNF) and interleukins (IL), are key mediators in the initiation and maintenance of chronic pain states. Sensory neurons expressing receptors for cytokines like TNF, IL-1, and IL-6 are implicated in peripheral sensitization, contributing to increased signaling of painful sensations. The potential of targeting TNF and IL for therapeutic intervention in chronic pain states is the focus of this review, with preclinical and clinical evidence supporting the use of TNF and IL modulators for pain management. The physiological and pathological roles of TNF in neuropathic pain is complex. Experimental evidence highlights the effectiveness of TNF modulation in mitigating pain symptoms in animal models and displays promising outcomes of clinical trials with TNF inhibitors, such as infliximab and etanercept. ILs, a diverse group of cytokines, including IL-1, IL-6, and IL-17, are discussed for their contributions to chronic pain through inflammation and peripheral sensitization. Specific IL modulators, such as secukinumab and tocilizumab, have shown potential in managing chronic neuropathic pain, as demonstrated in various studies and clinical trials. The pharmacokinetics, safety profiles, and challenges associated with TNF and IL modulators highlight the need for cautious medication monitoring in clinical practice. Comparative evaluations have revealed distinct efficacy and safety profiles among different cytokine modulators, emphasizing the need for personalized approaches based on the specific underlying causes of pain. Further research is necessary to elucidate the intricate mechanisms by which cytokines contribute to chronic pain, as well as to understand why they may affect pain differently in various contexts. Additionally, long-term safety profiles of cytokine modulators require more thorough investigation. This continued exploration holds the promise of enhancing our comprehension of cytokine modulation in chronic pain and shaping more potent therapeutic strategies for the future.
摘要：
慢性疼痛,复杂而衰弱的状况，涉及中枢和外周炎症过程之间复杂的相互作用。细胞因子,特别是肿瘤坏死因子（TNF）和白细胞介素（IL），是慢性疼痛状态开始和维持的关键介质。表达细胞因子如TNF受体的感觉神经元，IL-1和IL-6与外周致敏有关，有助于增加疼痛感觉的信号。靶向TNF和IL用于慢性疼痛状态的治疗干预的潜力是这篇综述的重点。临床前和临床证据支持使用TNF和IL调节剂进行疼痛管理。TNF在神经性疼痛中的生理和病理作用是复杂的。实验证据强调了TNF调节在减轻动物模型疼痛症状方面的有效性，并显示了使用TNF抑制剂的临床试验的有希望的结果。如英夫利昔单抗和依那西普。ILs,一组不同的细胞因子，包括IL-1，IL-6和IL-17，讨论了它们通过炎症和外周敏化对慢性疼痛的贡献。特异性IL调节剂,例如苏金单抗和托珠单抗，已经显示出治疗慢性神经性疼痛的潜力，正如在各种研究和临床试验中所证明的那样。药代动力学，安全概况,与TNF和IL调节剂相关的挑战凸显了临床实践中谨慎用药监测的必要性.比较评估显示不同细胞因子调节剂之间的不同疗效和安全性。强调需要基于疼痛的具体根本原因的个性化方法。需要进一步的研究来阐明细胞因子导致慢性疼痛的复杂机制。以及理解为什么它们在各种情况下对疼痛的影响不同。此外,细胞因子调节剂的长期安全性需要更彻底的研究.这种持续的探索有望增强我们对慢性疼痛中细胞因子调节的理解，并为未来制定更有效的治疗策略。
