Lung Barrier Function in COVID-19?
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COVID-19
Lung Barrier Function in COVID-19? T. K. Sivabakya 1
&
G. Srinivas 1
Accepted: 21 July 2020 / Published online: 18 August 2020 # Springer Nature Switzerland AG 2020
Abstract The novel coronavirus COVID-19 appears to strike some people more intensely than others. Some people only experience mild symptoms while others require hospitalization and ventilation. With the virus becoming more prevalent day by day, it is not just the elderly, but even young people are falling seriously ill. Various researchers across the world state that specific cells in the nasal passages, intestines, and lungs may be more susceptible to the infection. Shifting the focus and research towards epithelium might provide new insight towards understanding COVID-19. This article is an overview of how epithelium permeability in COVID-19 may associate with comorbidities and other factors. Keywords COVID - 19 . Epithelial barrier . Lung function . Mortality rate . Immune response . Inflammatory actions . Comorbidities . Epithelial permeability
Epithelium and Immunity
Pathogenesis of SARS-CoV-2
For decades, epithelial cells in innate immunity have been known to prevent the growth of bacterial and other microorganisms in the mucosal membrane [1]. Gong et al. [2] in his study shows that besides its mucociliary clearance feature, epithelial cells are now known to kill or neutralize microorganisms by producing many molecular families. Epithelial cells play a significant role in immune response regulation, inflammation, and host response. Although the role varies depending upon the pathogens and antigens, most of the diseases have a common pathology that includes marked epithelial cell activation in the upper airways or lower airways or both. Accumulating evidence by Schleimer et al. [3] suggests that epithelial cells are essential in initiating, regulating and maintaining the airway’s innate and adaptive immune response.
This article is part of the Topical Collection on Covid-19
The inhaled SARS-CoV-2 virus likely begins the replication on attachment to the epithelial cells in the nasal cavity. Angiotensin-converting enzyme 2 (ACE2) is the primary receptor for SARS-CoV2 and SARS-CoV. The virus spreads locally but has a minimal innate immune response. At this point, nasal swabs will detect the virus [4, 5]. These individuals are infectious although the viral burden may be low. Clinically manifested at this time is the COVID-19 disease. Viral epithelial infected cells are an important source of beta and lambda interferons [6]. Determining the innate immune response of the host may improve predictions of the disease’s subsequent course, and may require more aggressive monitoring. The disease would be mild for about 80% of the infected patients and mainly confined to the upper and conductive airways. Unfortunately, about 20% of the patients infected will advance to stage 3 disease and develop pulmonary infiltration, some of which will develop a very serious disease. So, the entire process starts when the virus infects the epithelial cells [
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