NLRP3-inflammasomes are triggered by age-related hearing loss in the inner ear of mice.

作者：Xi Shi, Shiwei Qiu, Wei Zhuang, Na Yuan, Caiji Wang, Shi‐Li Zhang, Tiantian Sun, Weiwei Guo, Fenglei Gao, Shiming Yang, Yuehua Qiao · 发表于：PubMed · 年份：2017 · 被引用次数：57 · 研究领域：Inflammasome and immune disorders、Immune Response and Inflammation、IL-33, ST2, and ILC Pathways

Age-related hearing loss (ARHL) or presbyacusis is a progressive loss of hearing sensitivity that is predominately associated with sensory or transduction neuro-cell degeneration in the peripheral and central auditory systems. Increased production of reactive oxygen species (ROS) and inflammatory response were frequently found in aging cochleae. In addition, inflammasomes are likely responsible for the accumulation of ROS in immune cells, although whether they are in fact involved in the development of ARHL is unknown. In this study, Q-PCR, WB and ELASA demonstrated significantly increased levels of activated Caspase-1, interleukin-1β and interleukin-18 and even NLRP3 in the inner ears of aging mice compared to younger one. In addition, NLRP3, as a sensor protein of ROS, may contribute to inflammasome assembly and subsequent inflammation in the cochleae. In conclusion, inflammation triggered by the activation of inflammasomes in the cochleae of aging mice appears to be playing an important role in the pathological process of ARHL and may be a potential cause of presbyacusis.