Age-associated changes in microglia-like and satellite glial cell markers in the cochlear spiral ganglion

Abstract Age-related hearing loss (ARHL) and noise-induced hearing loss (NIHL) are the most prevalent forms of acquired auditory impairment. However, whether the cochlear immune microenvironment differs between these conditions, and whether it can be therapeutically modulated, remains largely unknown. Satellite glial cells (SGCs), which ensheath spiral ganglion (SG) neurons, have not traditionally been considered immune-competent, and their role in cochlear immune remodeling has not been examined. Iba1⁺ microglia-like cells and Sox2⁺ SGCs were systematically characterized across four groups: young control (CTRL), young NIHL, aged vehicle-treated (Veh), and aged PLX5622-treated (PLX) mice, using double immunofluorescence staining for Iba1, Tmem119, Sox2, and CD74. In young mice, NIHL did not significantly alter total Iba1⁺ cell density or Iba1⁺/CD74⁺ co-expression in the SG compared to CTRL. In contrast, aged Veh mice showed a significant increase in total Iba1⁺ cell density and in Iba1 + /Tmem119 + , Iba1⁺/CD74⁺ and Sox2⁺/CD74⁺ cell densities relative to CTRL, with a similar upward trend for Sox2⁺/Tmem119⁺ cells that did not reach statistical significance after multiple-comparison correction. A 7-day course of the PLX5622 significantly reduced total Iba1⁺, Iba1 + /Tmem119 + , Iba1⁺/CD74⁺, and Sox2⁺/CD74⁺ cell densities in aged PLX mice. These findings identify age-associated differences in immune- and glia-associated marker-positive cell densities within the cochlear SG and show that selected marker-positive populations were reduced following PLX5622 treatment. Although age and genotype were confounded and PLX5622 may exert both local and systemic effects, these observations highlight the cochlear SG immune microenvironment as a potential area for further investigation in ARHL.