olfactory neuroepithelium
Recently Published Documents


TOTAL DOCUMENTS

106
(FIVE YEARS 30)

H-INDEX

24
(FIVE YEARS 3)

2021 ◽  
Vol 53 ◽  
pp. S660
Author(s):  
A. Delgado Sequera ◽  
M. Hidalgo-Figueroa ◽  
C. García-Mompó ◽  
J.M. Montesinos ◽  
J.I. Pérez-Revuelta ◽  
...  

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
B.-Y. Kim ◽  
J.Y. Park ◽  
K.J. Cho ◽  
J.H. Bae

Background: Urban particulate matter (UPM) in ambient air is implicated in a variety of human health issues worldwide, however, few studies exist on the effect of UPM on the olfactory system. This study aimed to identify the factors affecting the destruction of the olfactory system in a mouse model following UPM exposure. Methods: Mice were divided into: control and four UPM-exposed groups (200 µg UPM at 1 and 2 weeks, and 400 µg UPM at 1 and 2 weeks [standard reference material 1649b; average particle diameter 10.5 μm]). The olfactory neuroepithelium was harvested for histologic examination, gene ontology, quantitative real-time polymerase chain reaction, and western blotting. Results: Compared to the control group, olfactory marker protein, Olfr1507, ADCY3, and GNAL mRNA levels were lower, and S-100, CNPase, NGFRAP1, BDNF, and TACR3 mRNA levels were higher in the olfactory neuroepithelium of the UPM groups. Moderately positive correlation was present between the 1- and 2-week groups. After analyzing the 200 and 400 UPM groups separately, the strength of the association between the 200 UPM 1- and 2-week groups was moderately positive. No differences was present in the neuroepithelial inflammatory marker levels between the UPM and control groups. Conclusions: UPM could have cytotoxic effects on the olfactory epithelium. The exposure time and particular concentration of UPM exposure could affect the degree of destruction of the olfactory neuroepithelium. The olfactory regeneration mechanism could be related to the neurotrophic factors, olfactory ensheathing cell stimulation, and trigeminal nerve support.


2021 ◽  
Vol 2 (12) ◽  
pp. 56-66
Author(s):  
Isabela Porto Silva Costa ◽  
Talita Trindade França ◽  
Ivelise Theresa Araujo Balby ◽  
Gustavo Henrique Campos de Sousa ◽  
Luis Alves de Pinho Segundo

Esthesioneuroblastoma is a rare neoplasm of the nervous system that appears in the paranasal cavities derived from the olfactory neuroepithelium,  located in the cribriform region of the nasal fossa, and can invade the sinuses of the face, skull base and orbital region. Kadish classification is the most widely used to stage it according to its extension. The symptomatology is unspecific, and it may present progressive unilateral nasal obstruction, epistaxis, anosmia, headache, sinusitis, diplopia, and orbital proptosis. The diagnosis is based on the lesion biopsy, immunohistochemistry, and ultrastructural findings. Excision of the tumor is described as the treatment of choice that may be associated with radiotherapy and chemotherapy. This is a case report of an olfactory esthesioneuroblastoma in a patient admitted to the hospital complaining of orbital proptosis who, after a computed tomography of the skull, showed a suspicious lesion. After the biopsy and the anatomopathological study, a protocol with neoadjuvant chemotherapy was initiated, with the subsequent excision of the tumor. Despite the lack of other symptoms, an advanced stage of the neoplasm was identified, which reflects the importance of investigating less common complaints and thus facilitating the diagnosis and early treatment. 


2021 ◽  
Vol 27 (S1) ◽  
pp. 2284-2286
Author(s):  
Subrata De ◽  
Swaraj Sarkar ◽  
Swasti Barman ◽  
Sk Samim Hossin

2021 ◽  
pp. 194589242110264
Author(s):  
Boo-Young Kim ◽  
Ju Y. Park ◽  
Kwang J. Cho ◽  
Jung H. Bae

Background Exposure to urban particulate matter (UPM) is linked to the aggravation of various health problems. Although the nasal cavity is the first barrier to encounter UPM, there is a lack of studies on the impact of UPM on the olfactory area. The purpose of this study was to investigate the cytotoxic effects of UPM on mouse olfactory epithelium, the underlying pathophysiology involved, and changes in cytokine levels. Methods Mice were divided into 4 groups: control, 400UPM (administered 400 µg UPM daily; standard reference material 1649b; average particle diameter 10.5 μm) 1week, 400UPM 2weeks, and recovery 1week after 400UPM 2weeks (n = 10, 6, 6, and 6, respectively). Olfactory function was evaluated by conducting a food-finding test once a week. The olfactory neuroepithelium was harvested for histologic examination, gene ontology, quantitative real-time polymerase chain reaction, and western blotting. Results Compared to those in the control group, olfactory marker protein, olfactory receptor 1507, adenylyl cyclase 3, and GNAL mRNA levels were lower and S-100, 2′,3′-cyclic nucleotide 30-phosphodiesterase, nerve growth factor receptor-associated protein, brain-derived neurotrophic factor, and tachykinin receptor mRNA levels were higher in the 400UPM group olfactory neuroepithelium. There were no significant differences in neuroepithelial inflammatory marker levels between the 400UPM and saline group. Conclusions UPM decreased olfactory function and might have cytotoxic effects on the olfactory epithelium. Olfactory ensheathing cells and trigeminal nerve might be related to the regeneration of the olfactory epithelium after olfactory destruction associated with UPM.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1690
Author(s):  
Elena A. Zelenova ◽  
Nikolay V. Kondratyev ◽  
Tatyana V. Lezheiko ◽  
Grigoriy Y. Tsarapkin ◽  
Andrey I. Kryukov ◽  
...  

A major problem in psychiatric research is a deficit of relevant cell material of neuronal origin, especially in large quantities from living individuals. One of the promising options is cells from the olfactory neuroepithelium, which contains neuronal progenitors that ensure the regeneration of olfactory receptors. These cells are easy to obtain with nasal biopsies and it is possible to grow and cultivate them in vitro. In this work, we used RNAseq expression profiling and immunofluorescence microscopy to characterise neurospheres-derived cells (NDC), that simply and reliably grow from neurospheres (NS) obtained from nasal biopsies. We utilized differential expression analysis to explore the molecular changes that occur during transition from NS to NDC. We found that processes associated with neuronal and vascular cells are downregulated in NDC. A comparison with public transcriptomes revealed a depletion of neuronal and glial components in NDC. We also discovered that NDC have several metabolic features specific to neuronal progenitors treated with the fungicide maneb. Thus, while NDC retain some neuronal/glial identity, additional protocol alterations are needed to use NDC for mass sample collection in psychiatric research.


2021 ◽  
pp. eabf8396
Author(s):  
Guilherme Dias de Melo ◽  
Françoise Lazarini ◽  
Sylvain Levallois ◽  
Charlotte Hautefort ◽  
Vincent Michel ◽  
...  

Whereas recent investigations have revealed viral, inflammatory and vascular factors involved in SARS-CoV-2 lung pathogenesis, the pathophysiology of neurological disorders in COVID-19 remains poorly understood. Olfactory and taste dysfunction are common in COVID-19, especially in mildly symptomatic patients. Here, we conducted a virologic, molecular, and cellular study of the olfactory neuroepithelium of seven patients with COVID-19 presenting with acute loss of smell. We report evidence that the olfactory neuroepithelium may be a major site of SARS-CoV2 infection with multiple cell types, including olfactory sensory neurons, support cells, and immune cells, becoming infected. SARS-CoV-2 replication in the olfactory neuroepithelium was associated with local inflammation. Furthermore, we showed that SARS-CoV-2 induced acute anosmia and ageusia in golden Syrian hamsters, lasting as long as the virus remained in the olfactory epithelium and the olfactory bulb. Finally, olfactory mucosa sampling from patients showing long-term persistence of COVID-19-associated anosmia revealed the presence of virus transcripts and of SARS-CoV-2-infected cells, together with protracted inflammation. SARS-CoV-2 persistence and associated inflammation in the olfactory neuroepithelium may account for prolonged or relapsing symptoms of COVID-19, such as loss of smell, which should be considered for optimal medical management of this disease.


2021 ◽  
Author(s):  
Mariano Carossino ◽  
Paige Montanaro ◽  
Aoife O’Connell ◽  
Devin Kenney ◽  
Hans Gertje ◽  
...  

ABSTRACTAnimal models recapitulating the distinctive features of severe COVID-19 are critical to enhance our understanding of SARS-CoV-2 pathogenesis. Transgenic mice expressing human angiotensin-converting enzyme 2 (hACE2) under the cytokeratin 18 promoter (K18-hACE2) represent a lethal model of SARS-CoV-2 infection. However, the cause(s) and mechanisms of lethality in this mouse model remain unclear. Here, we evaluated the spatiotemporal dynamics of SARS-CoV-2 infection for up to 14 days post-infection. Despite infection and moderate inflammation in the lungs, lethality was invariably associated with viral neuroinvasion and neuronal damage (including spinal motor neurons). Neuroinvasion occurred following virus transport through the olfactory neuroepithelium in a manner that was only partially dependent on hACE2. Interestingly, SARS-CoV-2 tropism was overall neither widespread among nor restricted to only ACE2-expressing cells. Although our work incites caution in the utility of the K18-hACE2 model to study global aspects of SARS-CoV-2 pathogenesis, it underscores this model as a unique platform for exploring the mechanisms of SARS-CoV-2 neuropathogenesis.SUMMARYCOVID-19 is a respiratory disease caused by SARS-CoV-2, a betacoronavirus. Here, we show that in a widely used transgenic mouse model of COVID-19, lethality is invariably associated with viral neuroinvasion and the ensuing neuronal disease, while lung inflammation remains moderate.


Sign in / Sign up

Export Citation Format

Share Document