The balance between efficient anti-inflammatory treatment and neuronal regeneration in the olfactory epithelium

作     者：Seo Young Chang Isaias Glezer 

作者机构：Department of BiochemistryEscola Paulista de MedicinaUniversidade Federal de SAo Paulo 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2018年第13卷第10期

页      面：1711-1714页

核心收录：

学科分类：1002[医学-临床医学] 100213[医学-耳鼻咽喉科学] 10[医学] 

基　　金：supported by research grants to IG from Fundacao de Amparo a Pesquisa do Estado de Sao Paulo(FAPESP 2007/53732-8) Conselho Nacional de Desenvolvimento Científico e Tecnológico(CNPq 484869/2012-4) CEPID Redoxoma(FAPESP 2013/07937-8) 

主　　题：anti-inflammatory drugs corticosteroids hyposmia inflammation rhinosinusitis olfactory epithelium sensory neurons cell proliferation 

摘      要：The sense of smell is important for human quality of life. This sophisticated sensorial system relies on the detection of odorant molecules that engage receptors expressed in the cilia of dedicated neurons that constitute the olfactory epithelium（OE）. Importantly, the OE is a highly active site of adult neurogenesis where short-lived neurons are efficiently replenished, even after massive neuronal cell loss. It is suggested that the degree of olfactory function recovery after OE injury may depend on the nature of the lesion（traumatic, chemical, infectious or inflammatory）, as well on the velocity of cellular regeneration. Topical steroidal anti-inflammatory drugs, such as glucocorticoids, are routinely prescribed for treating upper airway inflammatory conditions, such as chronic rhinosinusitis. While the therapeutic strategy aims to minimize the inflammatory damage and dysfunction to nasal air conduction, new evidences raise concerns if such drugs may impair neuronal regeneration in the OE. In consequence, new directions are necessary in terms of drug development or prescription, in order to preserve olfactory function through lifelong repeated episodes of chronic inflammation in the upper respiratory tract. Here we discuss mechanisms involved in glucocorticoid deleterious effects to OE regeneration and possible therapeutic alternatives considering relevant side effects.