Inoculation of lymphocytes from young mice prevents progression of age-related hearing loss in a senescence-associated mouse model

Despite the increase in age-related hearing loss (ARHL) prevalence owing to increased population aging, pre-ventive 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 communi-cation 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 im-mune 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.

Automated summary

This study aimed to determine whether immuno-rejuvenation procedures can prevent age-related hearing loss (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 and their cryopreservation and inoculation at the onset of ARHL suggests their clinical application. This treatment not only maintained auditory threshold but also prevented spinal ganglion degeneration, cellular immune aging, and nitric oxide production, which causes age-related tissue damage.