Age-Related Hearing Loss: The Link between Inflammaging, Immunosenescence, and Gut Dysbiosis

Int J Mol Sci. 2022 Jul 1;23(13):7348. doi: 10.3390/ijms23137348.

Abstract

This article provides a theoretical overview of the association between age-related hearing loss (ARHL), immune system ageing (immunosenescence), and chronic inflammation. ARHL, or presbyacusis, is the most common sensory disability that significantly reduces the quality of life and has a high economic impact. This disorder is linked to genetic risk factors but is also influenced by a lifelong cumulative effect of environmental stressors, such as noise, otological diseases, or ototoxic drugs. Age-related hearing loss and other age-related disorders share common mechanisms which often converge on low-grade chronic inflammation known as "inflammaging". Various stimuli can sustain inflammaging, including pathogens, cell debris, nutrients, and gut microbiota. As a result of ageing, the immune system can become defective, leading to the accumulation of unresolved inflammatory processes in the body. Gut microbiota plays a central role in inflammaging because it can release inflammatory mediators and crosstalk with other organ systems. A proinflammatory gut environment associated with ageing could result in a leaky gut and the translocation of bacterial metabolites and inflammatory mediators to distant organs via the systemic circulation. Here, we postulate that inflammaging, as a result of immunosenescence and gut dysbiosis, accelerates age-related cochlear degeneration, contributing to the development of ARHL. Age-dependent gut dysbiosis was included as a hypothetical link that should receive more attention in future studies.

Keywords: age-related hearing loss; gut dysbiosis; immunosenescence; inflammation; presbyacusis.

Publication types

  • Review

MeSH terms

  • Aging / metabolism
  • Dysbiosis / microbiology
  • Humans
  • Immunosenescence*
  • Inflammation / metabolism
  • Inflammation Mediators
  • Presbycusis* / etiology
  • Quality of Life

Substances

  • Inflammation Mediators