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Respiratory epithelial cell responses to SARS-CoV-2 in COVID-19
Thorax ( IF 9.0 ) Pub Date : 2022-02-01 , DOI: 10.1136/thoraxjnl-2021-217561
James P Bridges 1, 2 , Eszter K Vladar 3 , Hua Huang 4 , Robert J Mason 5
Affiliation  

COVID-19 has different clinical stages, and effective therapy depends on the location and extent of the infection. The purpose of this review is to provide a background for understanding the progression of the disease throughout the pulmonary epithelium and discuss therapeutic options. The prime sites for infection that will be contrasted in this review are the conducting airways and the gas exchange portions of the lung. These two sites are characterised by distinct cellular composition and innate immune responses, which suggests the use of distinct therapeutic agents. In the nose, ciliated cells are the primary target cells for SARS-CoV-2 viral infection, replication and release. Infected cells shed their cilia, which disables mucociliary clearance. Evidence further points to a suppressed or incompletely activated innate immune response to SARS-CoV-2 infection in the upper airways. Asymptomatic individuals can still have a productive viral infection and infect others. In the gas exchange portion of the lung, the alveolar type II epithelial cell is the main target cell type. Cell death and marked innate immune response during infection likely contribute to alveolar damage and resultant acute respiratory distress syndrome. Alveolar infection can precipitate a hyperinflammatory state, which is the target of many therapies in severe COVID-19. Disease resolution in the lung is variable and may include scaring and long-term sequalae because the alveolar type II cells are also progenitor cells for the alveolar epithelium.

中文翻译:

COVID-19 中呼吸道上皮细胞对 SARS-CoV-2 的反应

COVID-19有不同的临床阶段,有效的治疗取决于感染的部位和程度。本综述的目的是为了解整个肺上皮的疾病进展提供背景,并讨论治疗方案。在本次审查中将对比的主要感染部位是肺的传导气道和气体交换部分。这两个部位的特点是不同的细胞组成和先天免疫反应,这表明使用不同的治疗剂。在鼻子中,纤毛细胞是 SARS-CoV-2 病毒感染、复制和释放的主要靶细胞。受感染的细胞会脱落纤毛,从而使粘液纤毛清除功能失效。有证据进一步表明,上呼吸道对 SARS-CoV-2 感染的先天免疫反应受到抑制或未完全激活。无症状的个体仍然可以产生有效的病毒感染并感染其他人。在肺的气体交换部分,肺泡II型上皮细胞是主要的靶细胞类型。感染期间的细胞死亡和显着的先天免疫反应可能导致肺泡损伤和导致的急性呼吸窘迫综合征。肺泡感染可诱发高炎症状态,这是严重 COVID-19 中许多疗法的目标。肺部疾病的消退是可变的,可能包括瘢痕和长期后遗症,因为肺泡 II 型细胞也是肺泡上皮的祖细胞。无症状的个体仍然可以产生有效的病毒感染并感染其他人。在肺的气体交换部分,肺泡II型上皮细胞是主要的靶细胞类型。感染期间的细胞死亡和显着的先天免疫反应可能导致肺泡损伤和导致的急性呼吸窘迫综合征。肺泡感染可诱发高炎症状态,这是严重 COVID-19 中许多疗法的目标。由于肺泡 II 型细胞也是肺泡上皮的祖细胞,因此肺部疾病的消退是可变的,可能包括瘢痕和长期后遗症。无症状的个体仍然可以产生有效的病毒感染并感染其他人。在肺的气体交换部分,肺泡II型上皮细胞是主要的靶细胞类型。感染期间的细胞死亡和显着的先天免疫反应可能导致肺泡损伤和导致的急性呼吸窘迫综合征。肺泡感染可诱发高炎症状态,这是严重 COVID-19 中许多疗法的目标。肺部疾病的消退是可变的,可能包括瘢痕和长期后遗症,因为肺泡 II 型细胞也是肺泡上皮的祖细胞。感染期间的细胞死亡和显着的先天免疫反应可能导致肺泡损伤和导致的急性呼吸窘迫综合征。肺泡感染可诱发高炎症状态,这是严重 COVID-19 中许多疗法的目标。由于肺泡 II 型细胞也是肺泡上皮的祖细胞,因此肺部疾病的消退是可变的,可能包括瘢痕和长期后遗症。感染期间的细胞死亡和显着的先天免疫反应可能导致肺泡损伤和导致的急性呼吸窘迫综合征。肺泡感染可诱发高炎症状态,这是严重 COVID-19 中许多疗法的目标。由于肺泡 II 型细胞也是肺泡上皮的祖细胞,因此肺部疾病的消退是可变的,可能包括瘢痕和长期后遗症。
更新日期:2022-01-12
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