Shuai Cheng1,2  · Qi Zhao1,2 · Guiyuan Rong3  · Shichu Sun1,2 · Hongjie Wang1,2 · Zhiyong Tan1  · Yonghua Ji1,2  · You Zhou1,2

1 Laboratory of Sensory Neurobiology, School of Basic Medical Sciences, Hebei University, Baoding 071002, China 

2 Key Laboratory of Aging and Health in Hebei Province, Baoding 071002, China 3 Department of Otorhinolaryngology, Affiliated Hospital of Hebei University, Baoding 071002, China

Abstract

Tinnitus is a common refractory disorder with complex mechanisms. Emerging evidence suggests that inflammation plays key roles in tinnitus pathogenesis; however, its overall inflammatory signatures remain underinvestigated. This study integrates transcriptomic data from patients with tinnitus and a noise-induced mouse model to identify conserved neuroinflammatory pathways. RNA sequencing of blood samples from patients with tinnitus and concurrent hearing loss revealed significant enrichment of immune-related pathways. Similar inflammatory signatures were detected through transcriptomic and cytokine profiling of the peripheral blood samples obtained from mice with noise-induced hearing loss. Microglial activation and elevated pro-inflammatory cytokines were observed in the cochlear nucleus and auditory cortex during the onset of noise-induced tinnitus. Pharmacological inhibition of microglial activation or tumor necrosis factor-α signaling alleviated tinnitus-like behaviors in mice. These findings reveal a dynamic peripheral-to-central inflammatory axis in tinnitus as well as identify blood-based biomarkers and auditory-center inflammation as potential therapeutic targets.

Keywords

Tinnitus; Neuroinflammation; Microglia; Cytokines; Noise-induced hearing loss; Therapeutic targets

[SpringerLink]