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Inflammation and Regeneration Alveolar Epithelial Cell Type II as main target of SARS-CoV-2 virus and COVID-19 development via NF-Kb pathway deregulation. Maurizio Carcaterra ( [email protected] ) Azienda Sanitaria Locale Vieterbo Belcolle Hospital Cristina Caruso Azienda Ospedaliera San Giovanni Addolorata Research Article Keywords: COVID-19, SARS-CoV-2, COVID-19 pathogenesis, NF-kB pathway activation, Alveolar Epitehlial Cell Type 2, AEC-II, ARDS. Posted Date: September 16th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-77539/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Version of Record: A version of this preprint was published on November 23rd, 2020. See the published version at https://doi.org/10.1016/j.mehy.2020.110412. Inflammation an d Regeneration Alveolar Epithelial Cell Type II as main target of SARS-CoV-2 virus and COVID-19 development via NF-Kb pathway deregulation. --Manuscript Draft-- Manuscript Number: IREG-D-20-00045 Full Title: Alveolar Epithelial Cell Type II as main target of SARS-CoV-2 virus and COVID-19 development via NF-Kb pathway deregulation. Article Type: Research article Section/Category: Inflammation Funding Information: Abstract: Background: The Corona Virus Disease (COVID-19) pandemic caused by Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2) requires a rapid solutionand global collaborative efforts in order to define preventive and treatment strategies. Methods: One of the major challenges of this disease is the high number of patients needing advanced respiratory support due to the Acute Respiratory Distress Syndrome (ARDS) as the lung is the major –although not exclusive-target of the virus. The molecular mechanisms, pathogenic drivers and the target cell type(s) in SARS- CoV-2 infection are still poorly understood, but the development of a “hyperactive” immune response is proposed to play a role in the evolution of the disease and it is envisioned as a major cause of morbidity and mortality. Results: Here we propose a theory by which the main targets for SARS-CoV-2 are the Type II Alveolar Epithelial Cells and the clinical manifestations of the syndrome are a direct consequence of their involvement. We hypotize the existence of a vicious cycle by which once alveolar damage starts in AEC II cells, the inflammatory state is supported by macrophage pro- inflammatory polarization (M1), cytokines release and by the activation of the NF-κB pathway. Conclusions: If this theory is confirmed, future therapeutic efforts can be directed to target Type 2 alveolar cells and the molecular pathogenic drivers associated with their dysfunction with currently available therapeutic strategies. Corresponding Author: MAURIZIO CARCATERRA Ospedale di Belcolle Viterbo, Lazio ITALY Corresponding Author E-Mail: [email protected];[email protected] Corresponding Author Secondary Information: Corresponding Author's Institution: Ospedale di Belcolle Corresponding Author's Secondary Institution: First Author: MAURIZIO CARCATERRA First Author Secondary Information: Order of Authors: MAURIZIO CARCATERRA Cristina Caruso Order of Authors Secondary Information: Opposed Reviewers: Additional Information: Question Response <b>Is this study a clinical No trial?</b><hr><i>A clinical trial is defined by the World Health Organisation as 'any research study that prospectively assigns human participants or groups of humans Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation to one or more health-related interventions to evaluate the effects on health outcomes'.</i> Are you submitting this manuscript to a Yes Thematic Series? Which Thematic Series? COVID-19: Its Pathogenetic Mechanisms and Potential Therapeutics as follow-up to "Are you submitting this manuscript to a Thematic Series?" Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation Title 1 Alveolar Epithelial Cell Type II as main target of SARS-CoV-2 virus and COVID-19 2 development via NF-Kb pathway deregulation. 3 4 Running Title 5 6 COVID-19 sustained by NF-Kb pathway deregulation 7 8 Keywords 9 10 COVID-19, SARS-CoV-2, COVID-19 pathogenesis, NF-kB pathway activation, 11 Alveolar Epitehlial Cell Type 2, AEC-II, ARDS. 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 1 Abstract: 2 3 Background: The Corona Virus Disease (COVID-19) pandemic caused by Severe 4 5 6 Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2) requires a rapid solution 7 8 and global collaborative efforts in order to define preventive and treatment strategies. 9 10 11 Methods: One of the major challenges of this disease is the high number of patients 12 13 needing advanced respiratory support due to the Acute Respiratory Distress Syndrome 14 15 (ARDS) as the lung is the major –although not exclusive- target of the virus. The 16 17 18 molecular mechanisms, pathogenic drivers and the target cell type(s) in SARS-CoV-2 19 20 infection are still poorly understood, but the development of a “hyperactive” immune 21 22 response is proposed to play a role in the evolution of the disease and it is envisioned as 23 24 25 a major cause of morbidity and mortality. 26 27 Results: Here we propose a theory by which the main targets for SARS-CoV-2 are the 28 29 Type II Alveolar Epithelial Cells and the clinical manifestations of the syndrome are a 30 31 32 direct consequence of their involvement. We hypotize the existence of a vicious cycle 33 34 by which once alveolar damage starts in AEC II cells, the inflammatory state is 35 36 supported by macrophage pro-inflammatory polarization (M1), cytokines release and by 37 38 39 the activation of the NF-κB pathway. 40 41 Conclusions: If this theory is confirmed, future therapeutic efforts can be directed to 42 43 target Type 2 alveolar cells and the molecular pathogenic drivers associated with their 44 45 46 dysfunction with currently available therapeutic strategies. 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 1 2 3 4 5 6 7 8 9 10 Graphical Abstract 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 Introduction: 38 39 In the past twenty years there have been precedents for epidemic clusters sustained by 40 41 viruses that have bats as their main hosts. The dynamic of the transmission from bat- 42 43 44 borne viruses to humans is very complex and often involves the presence of additional 45 46 intermediate hosts [1–3]. The human Coronavirus (hCoV) family belongs to a well- 47 48 recognized bat-borne family of viruses that infects humans causing predominant 49 50 51 damage to the respiratory system strictly connected with the development of ARDS [4, 52 53 5]. Previous Coronavirus-mediated diseases are Severe Acute Respiratory Syndrome 54 55 56 Coronavirus (SARS-Co-V) or Middle East Respiratory Syndrome CoV (MERS CoV) 57 58 [6–8] closely related to the new SARS-CoV-2 responsible for Coronavirus Disease 19 59 60 (COVID-19) [1, 9–11]. ARDS is a manifestation of lung injury, therefore not a disease 61 62 63 64 65 itself, rather a syndrome induced by different insults and characterized by substantial 1 2 heterogeneity [4, 5]. We propose the hypothesis that the main target of the virus is the 3 4 Alveolar Epithelial Cell Type II and that a dysregulation of the Nuclear Factor kappa- 5 6 light-chain-enhancer of activated B cells pathway (NF-κB pathway) drives ARDS 7 8 9 leading to Multiple Organ Failure (MOF), one of the most frequent causes of death. By 10 11 correlating the clinical data and examining the pathophysiology of the various diseases 12 13 present in COVID-19, we focused our attention on the intra and extra cellular signaling 14 15 16 mechanisms that are activated following damage at the alveolar level and on how these 17 18 signals are distantly propagated and amplified. 19 20 21 Discussion: 22 23 When a pathogen like a virus infects humans, the immune system could clear the 24 25 infection by limiting viral spread (effective antiviral response), or cause an excessive 26 27 28 inflammation and tissue destruction by cytotoxic cells and consequent development of 29 30 immuno-pathological damage. The epithelial cells are critical for balancing these two 31 32 extreme situations [12]. The upper respiratory tract provides the first line of defense in 33 34 35 that it activates a very complex system of signaling and recruitment of immune cells, in 36 37 order to prevent pathogens from reaching the alveoli, the most important part of the 38 39 respiratory system because responsible of gas exchange. Nevertheless, coronaviruses 40 41 42 (especially SARS-CoV and MERS) are able to reduce or delay the expression of 43 44 cytokines in human lung epithelial cell lines. This is an effective system to escape 45 46 immune recognition by innate receptors in the infected cell [13, 14], which could 47 48 49 therefore facilitate the progression of the virus into the lower respiratory airways (i.e. 50 51 the alveolar space) (Fig.1). 52 53 54 55 56 57 58 59 60 61 These observations are coherent with some clinical evidence of CoVID-19 as well: 1) A 62 63 64 65 high number of asymptomatic patients are positive at the nasopharyngeal swab for virus 1 2 detection with real-time reverse transcription (RT)-PCR, which strongly suggests that 3 4 despite viral load is present, no symptoms occur due to the lack of innate immune 5 6 response; 2) On the other hand, in mild symptomatic patients –some time negative with 7 8 9 nasopharyngeal swab-, early alveolar damage can still be detected with CT scan [15], 10 11 thus demonstrating that the first and most important site of damage is the lung 12 13 parenchyma.
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