Inflammation in hearing loss


Several studies support the idea that inflammatory responses are associated with drug-, noise- and age-related hearing loss.

Drug-related hearing loss is defined as a temporary or permanent inner ear dysfunction after drug exposure, and it is one of the most preventable causes of deafness (although the toxicity of some drugs is well known, they are used because in many cases their benefits outweigh their negative side effects). Some drugs produce inflammatory responses in the inner ear.

In noise-related hearing loss, a frequently a predictable form of hearing loss, there are inflammatory responses in the cochlea (the part of the inner ear that contains the endings of the nerve that carries information about sound to the brain) following exposure to traumatic noise.

Age-related hearing loss is the most common form of hearing loss in adults. It is due to a combination of environmental and genetic factors, but another key factor is the state of chronic inflammation in the elderly, which is a consequence of the aging of the immune system.

Decades of research have not delivered effective strategies for preventing or ameliorating these types of hearing loss, and the most common therapies have inconsistent results. However, recent advances in the understanding of the resolution of inflammation suggest potential therapeutic strategies (based on the improvement of the resolution of inflammatory responses) that might be useful in preventing cochlear damage produced by inflammation. Improving the resolution phase of inflammatory responses in the inner ear may naturally contribute to the prevention or amelioration of auditory dysfunctions.



Specialized pro-resolving mediators I – How does inflammation work?

Specialized pro-resolving mediators II – What are the specialized pro-resolving mediators?

Kalinec GM, Lomberk G, Urrutia RA, Kalinec F. Resolution of Cochlear Inflammation: Novel Target for Preventing or Ameliorating Drug-, Noise- and Age-related Hearing Loss. Front Cell Neurosci. 2017 Jul 7;11:192.


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