Inflammatory Signatures of Tinnitus in Patients and Mice.

Summary

RNA sequencing of blood samples from tinnitus patients with concurrent hearing loss showed enrichment of immune-related pathways; the same inflammatory signature appeared in blood and cytokine profiling from a mouse model of noise-induced hearing loss. In mice, microglial activation and elevated pro-inflammatory cytokines appeared in the cochlear nucleus and auditory cortex around tinnitus onset, and pharmacologically blocking microglial activation or TNF-alpha signaling reduced tinnitus-like behavior. Proposes a peripheral-to-central inflammatory axis in tinnitus, with blood-based biomarker and anti-inflammatory therapeutic potential.

Key findings

• Blood RNA-seq shows the same inflammatory pathway enrichment in tinnitus patients and in a mouse noise-exposure model.
• Microglial activation and elevated pro-inflammatory cytokines appear in the cochlear nucleus and auditory cortex at tinnitus onset.
• Pharmacologically blocking microglial activation or TNF-alpha signaling reduced tinnitus-like behavior in mice.
• Proposes a peripheral-to-central inflammatory axis, with blood-based biomarker potential.