Age-related hearing loss (ARHL) does not have established preventive measures.

Inoculation of cryopreserved lymphocytes from young mice led to immune regeneration.

This immune manipulation inhibited ARHL progression in aged mice.

Cochlear atrophy and oxidative stress were also suppressed in the hosts.

Autologous lymphocyte inoculation may have clinical application in ARHL prevention.

Despite the increase in age-related hearing loss (ARHL) prevalence owing to increased population aging, preventive measures against ARHL have not yet been established. The immune system becomes one of the most dysfunctional systems upon aging, and immunosenescence greatly affects homeostasis and promotes systemic aging along with chronic inflammation and oxidative stress. This study aimed to determine whether immuno-rejuvenation procedures can prevent ARHL and have clinical applications as well as to analyze the communication mechanisms between the systemic immune system and the cochlea using a murine model. Lymphocytes from young mice inhibited the progression of ARHL. The method of cryopreserving these lymphocytes and inoculating them at the onset of ARHL suggests their clinical application. Mice that were administered this treatment not only maintained auditory threshold but also avoided spinal ganglion degeneration, cellular immune aging, and nitric oxide production, which causes age-related tissue damage. These findings coincide with our previous strategies against immunosenescence and neuronal aging. Therefore, the manipulation of systemic immune function may contribute not only to the prevention of ARHL but also to the development of novel anti-aging clinical measures, paving the way to healthy longevity with preserved organ function.

Hearing loss

Nitric oxide

Rejuvenation

Senescence

Spiral ganglion

T lymphocytes

Auditory brainstem response

Age-related hearing loss

Fluorescein isothiocyanate

Inducible nitric oxide synthase

Idiopathic sudden sensorineural hearing loss

Naturally occurring regulatory T cell

Reactive oxygen species

Senescence-associated secretory phenotype

© 2023 The Authors. Published by Elsevier Inc.