The International Tinnitus Journal

The International Tinnitus Journal

Official Journal of the Neurootological and Equilibriometric Society
Official Journal of the Brazil Federal District Otorhinolaryngologist Society

Reach Us Reach Us Whatsapp +44 7367 141882

ISSN: 0946-5448

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Abstract

The Role of Gut Dysbiosis in the Pathophysiology of Tinnitus: A Literature Review

Author(s): Imam Megantara, Gisela Liani Wikargana,Yussy Afriani Dewi, Agung Dinasti Permana, Nova Sylviana

Introduction: For years, tinnitus has become a prevalent symptom in the ENT department. However, the mechanism underlying tinnitus remains unclear. There is increasing evidence that tinnitus is related to an abnormal central gain in the central auditory system and increased neuroinflammatory mediators. On the other hand, recent studies have shown that gut dysbiosis plays a crucial role in brain function, and gut dysbiosis contributes to several neurological diseases. Hence, giving insight into its possible involvement in tinnitus.

Aim: This study evaluated the potential role of gut microbiota dysbiosis in the path mechanism of tinnitus, mainly through its effect on neurotransmitter production and neuroinflammation induction.

Methods: This study uses a literature review approach, inclusive only of experimental studies in the recent five years discussing gut dysbiosis, neurotransmitter, neuroinflammation, and tinnitus signaling. Results: From 22 relevant literature, we found that gut dysbiosis impacts neurotransmitter production such as GABA and 5-HT and contributes to the neuroinflammatory process by increasing pro-inflammatory cytokines and activated microglia. These altered neurotransmitter profiles and triggered pro-inflammatory mediators were also found in tinnitus.

Conclusion: Gut microbiota dysbiosis is likely to underlie tinnitus’s pathomechanism by altering neurotransmitter production and activating the neuroinflammatory response in the brain.

Text PDF

Share this  Facebook  Twitter  LinkedIn  Google+