Dept. Biomedical Engineering, Fitzpatrick Center (FCIEMAS), 101 Science Drive, Campus Box 90281, Duke University, Durham, NC 27708-0281, USA; Global Center for Hearing & Speech Res., 3802 Spectrum Blvd., BPB Suite 210, University of South Florida Res. Park, Tampa, FL 33612, USA; Dept. Chemical & Biomedical Engineering, 4202 E Fowler Avenue, ENB 118 University of South Florida, Tampa, FL 33620, USA.
Dept. Communication Sciences & Disorders, 4202 E. Fowler Avenue, PCD1017 University of South Florida, Tampa, FL 33620-8200, USA; Global Center for Hearing & Speech Res., 3802 Spectrum Blvd., BPB Suite 210, University of South Florida Res. Park, Tampa, FL 33612, USA.
Ageing Res Rev. 2017 Nov;40:142-148. doi: 10.1016/j.arr.2017.10.002. Epub 2017 Oct 7.
Chronic, low-grade inflammation, or inflammaging, is a crucial contributor to various age-related pathologies and natural processes in aging tissue, including the nervous system. Over the past two decades, much effort has been done to understand the mechanisms of inflammaging in disease models such as type II diabetes, cardiovascular disease, Alzheimer's disease, Parkinson's disease, and others. However, despite being the most prevalent neurodegenerative disorder, the number one communication disorder, and one of the top three chronic medical conditions of our aged population; little research has been conducted on the potential role of inflammation in age-related hearing loss (ARHL). Recently, it has been suggested that there is an inflammatory presence in the cochlea, perhaps involving diffusion processes of the blood-brain barrier as it relates to the inner ear. Recent research has found correlations between hearing loss and markers such as C-reactive protein, IL-6, and TNF-α indicating inflammatory status in human case-cohort studies. However, there have been very few reports of in vivo research investigating the role of chronic inflammation's in hearing loss in the aging cochlea. Future research directed at better understanding the mechanisms of inflammation in the cochlea as well as the natural changes acquired with aging may provide a better understanding of how this process can accelerate presbycusis. Animal model experimentation and pre-clinical studies designed to recognize and characterize cochlear inflammatory mechanisms may suggest novel treatment strategies for preventing or treating ARHL. In this review, we seek to summarize key research in chronic inflammation, discuss its implications for possible roles in ARHL, and finally suggest directions for future investigations.
慢性、低度炎症，或炎症衰老，是各种与年龄相关的病理和衰老组织（包括神经系统）自然过程的关键因素。在过去的二十年中，人们做出了很多努力来理解炎症衰老在疾病模型中的机制，如 2 型糖尿病、心血管疾病、阿尔茨海默病、帕金森病等。然而，尽管听力损失是最常见的神经退行性疾病、头号交流障碍，也是老年人群中三大慢性疾病之一，但针对炎症在年龄相关性听力损失（ARHL）中的潜在作用的研究却很少。最近，有人提出耳蜗中存在炎症，可能涉及血脑屏障的扩散过程，这与内耳有关。最近的研究发现，听力损失与 C 反应蛋白、IL-6 和 TNF-α 等标志物之间存在相关性，这表明在人类病例队列研究中存在炎症状态。然而，很少有关于体内研究调查慢性炎症在衰老耳蜗中听力损失作用的报道。未来针对更好地理解耳蜗中炎症机制以及与衰老相关的自然变化的研究，可能会更好地理解这一过程如何加速 presbycusis。旨在识别和表征耳蜗炎症机制的动物模型实验和临床前研究可能会为预防或治疗 ARHL 提供新的治疗策略。在这篇综述中，我们试图总结慢性炎症的关键研究，讨论其对 ARHL 可能作用的影响，并最后提出未来研究的方向。
