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Massive transient damage of the olfactory epithelium associated with infection of sustentacular cells by SARS-CoV-2 in golden Syrian hamsters
Brain, Behavior, and Immunity ( IF 8.8 ) Pub Date : 2020-10-01 , DOI: 10.1016/j.bbi.2020.06.032
Bertrand Bryche 1 , Audrey St Albin 1 , Severine Murri 2 , Sandra Lacôte 2 , Coralie Pulido 3 , Meriadeg Ar Gouilh 4 , Sandrine Lesellier 5 , Alexandre Servat 5 , Marine Wasniewski 5 , Evelyne Picard-Meyer 5 , Elodie Monchatre-Leroy 5 , Romain Volmer 6 , Olivier Rampin 7 , Ronan Le Goffic 1 , Philippe Marianneau 2 , Nicolas Meunier 1
Affiliation  

Abstract Anosmia is one of the most prevalent symptoms of SARS-CoV-2 infection during the COVID-19 pandemic. However, the cellular mechanism behind the sudden loss of smell has not yet been investigated. The initial step of odour detection takes place in the pseudostratified olfactory epithelium (OE) mainly composed of olfactory sensory neurons surrounded by supporting cells known as sustentacular cells. The olfactory neurons project their axons to the olfactory bulb in the central nervous system offering a potential pathway for pathogens to enter the central nervous system by bypassing the blood brain barrier. In the present study, we explored the impact of SARS-COV-2 infection on the olfactory system in golden Syrian hamsters. We observed massive damage of the OE as early as 2 days post nasal instillation of SARS-CoV-2, resulting in a major loss of cilia necessary for odour detection. These damages were associated with infection of a large proportion of sustentacular cells but not of olfactory neurons, and we did not detect any presence of the virus in the olfactory bulbs. We observed massive infiltration of immune cells in the OE and lamina propria of infected animals, which may contribute to the desquamation of the OE. The OE was partially restored 14 days post infection. Anosmia observed in COVID-19 patient is therefore likely to be linked to a massive and fast desquamation of the OE following sustentacular cells infection with SARS-CoV-2 and subsequent recruitment of immune cells in the OE and lamina propria.

中文翻译:


金色叙利亚仓鼠中与支持细胞感染 SARS-CoV-2 相关的嗅觉上皮的大规模短暂损伤



摘要 嗅觉丧失是 COVID-19 大流行期间 SARS-CoV-2 感染最常见的症状之一。然而,嗅觉突然丧失背后的细胞机制尚未得到研究。气味检测的第一步发生在假复层嗅上皮 (OE),主要由嗅觉感觉神经元组成,周围环绕着支持细胞(支持细胞)。嗅觉神经元将其轴突投射到中枢神经系统的嗅球,为病原体绕过血脑屏障进入中枢神经系统提供了潜在的途径。在本研究中,我们探讨了 SARS-COV-2 感染对金色叙利亚仓鼠嗅觉系统的影响。早在鼻腔滴注 SARS-CoV-2 后 2 天,我们就观察到 OE 出现严重损伤,导致气味检测所需的纤毛大量损失。这些损伤与大部分支持细胞的感染有关,但与嗅觉神经元的感染无关,而且我们没有在嗅球中检测到任何病毒的存在。我们观察到受感染动物的外皮和固有层中免疫细胞大量浸润,这可能导致外皮剥落。感染后 14 天,OE 部分恢复。因此,在 COVID-19 患者中观察到的嗅觉丧失可能与支持细胞感染 SARS-CoV-2 以及随后在 OE 和固有层中招募免疫细胞后 OE 的大量快速脱皮有关。
更新日期:2020-10-01
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