![]() Not surprisingly, when the timely resolution of inflammation fails, it progresses to chronic inflammation, a condition that can persist for months and even years (Figure 1). At the front line of the host defense mechanism is acute inflammation, a short-term physiologic response aimed to return, at least in part, the organism to the normal phenotype. Mammals are able to detect the presence of pathogen agents and tissue injury, and initiate complex tissue repair and wound healing programs. Therefore, rather than to prevent inflammation, any clinical strategy should be aimed at facilitating its rapid, safe and complete resolution. ![]() Moreover, inflammation can help to establish an immunological memory that the organism can use later to generate a better response to a particular infectious agent ( Gilroy and De Maeyer, 2015 Headland and Norling, 2015). The most important paradigm recognized and highlighted in this article is that inflammation in any tissue, organ and system, behaves as a beneficial host reaction aimed at protecting individuals from infections and tissue injury. ![]() ![]() Since these studies suggest that improving the resolution process could be useful for the prevention of inflammation-associated diseases in humans, we discuss the potential application of similar strategies to prevent or mitigate DRHL, NRHL and ARHL. In particular, we emphasize beneficial approaches that have been tested in pre-clinical models of inflammatory responses induced by recognized ototoxic drugs such as cisplatin and aminoglycoside antibiotics. In this review article, we describe recent advances in the understanding of the resolution phase of inflammation and highlight therapeutic strategies that might be useful in preventing inflammation-induced cochlear damage. Inflammation by itself produces specialized pro-resolving mediators with critical functions, including essential fatty acid derivatives (lipoxins, resolvins, protectins and maresins), proteins and peptides such as annexin A1 and galectins, purines (adenosine), gaseous mediators (NO, H 2S and CO), as well as neuromodulators like acetylcholine and netrin-1. The resolution of inflammation is not a passive response but rather an active, highly controlled and coordinated process. Therefore, an appropriate approach to prevent or ameliorate DRHL, NRHL and ARHL should involve improving the resolution of the inflammatory process in the cochlea rather than inhibiting this phenomenon. Inflammation, however, is a normal adaptive response aimed at restoring tissue functionality and homeostasis after infection, tissue injury and even stress under sterile conditions, and suppressing it could have unintended negative consequences. ![]() Consequently, several clinical strategies aimed at reducing auditory dysfunction by preventing inflammation are currently under intense scrutiny. 2Epigenetics and Chromatin Dynamics Laboratory, Translational Epigenomic Program, Center for Individualized Medicine (CIM) Mayo Clinic, Rochester, MN, United StatesĪ significant number of studies support the idea that inflammatory responses are intimately associated with drug-, noise- and age-related hearing loss (DRHL, NRHL and ARHL).1Laboratory of Auditory Cell Biology, Department of Head and Neck Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States. ![]()
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