Apoptosis and turnover disruption of olfactory sensory neurons in eosinophilic chronic rhinosinusitis

Abstract

Olfactory dysfunction (OD) is one of the important and difficult-to-treat symptoms of eosinophilic chronic rhinosinusitis (CRS), which is typically associated with type 2 inflammation where eosinophils (EOSs) function as both effectors and initiators. Eosinophilic infiltration in the olfactory mucosa (OM) is associated with severe OD, mucosal erosion, and more loss of olfactory sensory neurons (OSNs). Active EOS-derived cytokines, chemokines, and eosinophil granule proteins may lead to aggravation of inflammation, tissue damage, and impairment of the survival and regeneration of OSNs. Recent studies show that EOSs can lead to apoptosis of OSNs through axonal and neural body damage, turnover disorder of OSNs through the loss of immature OSNs and globose basal cells (GBCs), changed proliferative activity of horizontal basal cells (HBCs), and dysfunction of OSNs through the breakdown of neuroepithelial integrity and alteration of ion concentration in OSNs and mucin. In this review, we outline the current progress on the role of EOSs on OD in patients with eosinophilic CRS and the mechanism of EOS-associated injury of the OM and OSNs in experimental animal models with sinonasal inflammation. Further investigations on the molecular mechanisms of tissue eosinophilia-induced injury of OSNs are warranted to obtain new therapeutic targets and achieve better restoration of olfactory function.

A Pilot Study on a Possible Mechanism behind Olfactory Dysfunction in Parkinson’s Disease: The Association of TAAR1 Downregulation with Neuronal Loss and Inflammation along Olfactory Pathway

“…Much like vision and hearing, the faculty of smell invariably declines with age [52], attributable to factors such as decreased regenerative capacity [53], cellular apoptosis [54], and disruptions in neural transmission [55]. Different from normal age-related olfactory decline, the above process is further exacerbated in PD patients due to neurodegenerative or other PD-related pathological lesions [16].…”

Incidence and influencing factors of olfactory dysfunction in patients 1 week after endoscopic transsphenoidal resection of pituitary tumor: a cross-sectional study of 158 patients

“…After transsphenoidal surgery, the olfactory epithelium and its surrounding mucosa may experience issues such as blood scab formation and structural changes ( 27 ), leading to physical blockage of airflow in the nasal cavity, preventing odor molecules from reaching the olfactory receptor neurons and impacting the recovery of olfactory function. Furthermore, eosinophilic infiltration may occur in the area of blood crust formation, resulting in prolonged exposure of the nasal mucosa to fungal extracts, leading to significant thinning of the olfactory epithelium and exacerbating the development of olfactory dysfunction ( 26 , 28 , 29 ). Koskinen et al ( 30 ) also found that the long-standing nasal blood scab may lead to chronic bacterial colonization, and further affecting the olfactory function.…”