Asthma Associated Cytokines Regulate the Expression of SARS-CoV-2 Receptor ACE2 in the Lung Tissue of Asthmatic Patients
It is still controversial whether chronic lung inflammation increases the risk for COVID-19. One of the risk factors for acquiring COVID-19 is the level of expression of SARS-CoV-2 entry receptors, ACE2 and TMPRSS2, in lung tissue. It is, however, not clear how lung tissue inflammation affects expre...
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| Published in | Frontiers in immunology Vol. 12; p. 796094 |
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| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Frontiers Media S.A
17.01.2022
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| Abstract | It is still controversial whether chronic lung inflammation increases the risk for COVID-19. One of the risk factors for acquiring COVID-19 is the level of expression of SARS-CoV-2 entry receptors, ACE2 and TMPRSS2, in lung tissue. It is, however, not clear how lung tissue inflammation affects expression levels of these receptors. We hence aimed to determine the level of SARS-CoV-2 receptors in lung tissue of asthmatic relative to age, gender, and asthma severity, and to investigate the factors regulating that. Therefore, gene expression data sets of well-known asthmatic cohorts (SARP and U-BIOPRED) were used to evaluate the association of ACE2 and TMPRSS2 with age, gender of the asthmatic patients, and also the type of the underlying lung tissue inflammatory cytokines. Notably, ACE2 and to less extent TMPRSS2 expression were upregulated in the lung tissue of asthmatics compared to healthy controls. Although a differential expression of ACE2, but not TMPRSS2 was observed relative to age within the moderate and severe asthma groups, our data suggest that age may not be a key regulatory factor of its expression. The type of tissue inflammation, however, associated significantly with ACE2 and TMPRSS2 expression levels following adjusting with age, gender and oral corticosteroids use of the patient. Type I cytokine (IFN-γ), IL-8, and IL-19 were associated with increased expression, while Type II cytokines (IL-4 and IL-13) with lower expression of ACE2 in lung tissue (airway epithelium and/or lung biopsies) of moderate and severe asthmatic patients. Of note, IL-19 was associated with ACE2 expression while IL-17 was associated with TMPRSS2 expression in sputum of asthmatic subjects.
In vitro
treatment of bronchial fibroblasts with IL-17 and IL-19 cytokines confirmed the regulatory effect of these cytokines on SARS-CoV-2 entry receptors. Our results suggest that the type of inflammation may regulate ACE2 and TMPRSS2 expression in the lung tissue of asthmatics and may hence affect susceptibility to SARS-CoV-2 infection. |
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| AbstractList | It is still controversial whether chronic lung inflammation increases the risk for COVID-19. One of the risk factors for acquiring COVID-19 is the level of expression of SARS-CoV-2 entry receptors, ACE2 and TMPRSS2, in lung tissue. It is, however, not clear how lung tissue inflammation affects expression levels of these receptors. We hence aimed to determine the level of SARS-CoV-2 receptors in lung tissue of asthmatic relative to age, gender, and asthma severity, and to investigate the factors regulating that. Therefore, gene expression data sets of well-known asthmatic cohorts (SARP and U-BIOPRED) were used to evaluate the association of ACE2 and TMPRSS2 with age, gender of the asthmatic patients, and also the type of the underlying lung tissue inflammatory cytokines. Notably, ACE2 and to less extent TMPRSS2 expression were upregulated in the lung tissue of asthmatics compared to healthy controls. Although a differential expression of ACE2, but not TMPRSS2 was observed relative to age within the moderate and severe asthma groups, our data suggest that age may not be a key regulatory factor of its expression. The type of tissue inflammation, however, associated significantly with ACE2 and TMPRSS2 expression levels following adjusting with age, gender and oral corticosteroids use of the patient. Type I cytokine (IFN-γ), IL-8, and IL-19 were associated with increased expression, while Type II cytokines (IL-4 and IL-13) with lower expression of ACE2 in lung tissue (airway epithelium and/or lung biopsies) of moderate and severe asthmatic patients. Of note, IL-19 was associated with ACE2 expression while IL-17 was associated with TMPRSS2 expression in sputum of asthmatic subjects.
In vitro
treatment of bronchial fibroblasts with IL-17 and IL-19 cytokines confirmed the regulatory effect of these cytokines on SARS-CoV-2 entry receptors. Our results suggest that the type of inflammation may regulate ACE2 and TMPRSS2 expression in the lung tissue of asthmatics and may hence affect susceptibility to SARS-CoV-2 infection. It is still controversial whether chronic lung inflammation increases the risk for COVID-19. One of the risk factors for acquiring COVID-19 is the level of expression of SARS-CoV-2 entry receptors, ACE2 and TMPRSS2, in lung tissue. It is, however, not clear how lung tissue inflammation affects expression levels of these receptors. We hence aimed to determine the level of SARS-CoV-2 receptors in lung tissue of asthmatic relative to age, gender, and asthma severity, and to investigate the factors regulating that. Therefore, gene expression data sets of well-known asthmatic cohorts (SARP and U-BIOPRED) were used to evaluate the association of ACE2 and TMPRSS2 with age, gender of the asthmatic patients, and also the type of the underlying lung tissue inflammatory cytokines. Notably, ACE2 and to less extent TMPRSS2 expression were upregulated in the lung tissue of asthmatics compared to healthy controls. Although a differential expression of ACE2, but not TMPRSS2 was observed relative to age within the moderate and severe asthma groups, our data suggest that age may not be a key regulatory factor of its expression. The type of tissue inflammation, however, associated significantly with ACE2 and TMPRSS2 expression levels following adjusting with age, gender and oral corticosteroids use of the patient. Type I cytokine (IFN-γ), IL-8, and IL-19 were associated with increased expression, while Type II cytokines (IL-4 and IL-13) with lower expression of ACE2 in lung tissue (airway epithelium and/or lung biopsies) of moderate and severe asthmatic patients. Of note, IL-19 was associated with ACE2 expression while IL-17 was associated with TMPRSS2 expression in sputum of asthmatic subjects. In vitro treatment of bronchial fibroblasts with IL-17 and IL-19 cytokines confirmed the regulatory effect of these cytokines on SARS-CoV-2 entry receptors. Our results suggest that the type of inflammation may regulate ACE2 and TMPRSS2 expression in the lung tissue of asthmatics and may hence affect susceptibility to SARS-CoV-2 infection.It is still controversial whether chronic lung inflammation increases the risk for COVID-19. One of the risk factors for acquiring COVID-19 is the level of expression of SARS-CoV-2 entry receptors, ACE2 and TMPRSS2, in lung tissue. It is, however, not clear how lung tissue inflammation affects expression levels of these receptors. We hence aimed to determine the level of SARS-CoV-2 receptors in lung tissue of asthmatic relative to age, gender, and asthma severity, and to investigate the factors regulating that. Therefore, gene expression data sets of well-known asthmatic cohorts (SARP and U-BIOPRED) were used to evaluate the association of ACE2 and TMPRSS2 with age, gender of the asthmatic patients, and also the type of the underlying lung tissue inflammatory cytokines. Notably, ACE2 and to less extent TMPRSS2 expression were upregulated in the lung tissue of asthmatics compared to healthy controls. Although a differential expression of ACE2, but not TMPRSS2 was observed relative to age within the moderate and severe asthma groups, our data suggest that age may not be a key regulatory factor of its expression. The type of tissue inflammation, however, associated significantly with ACE2 and TMPRSS2 expression levels following adjusting with age, gender and oral corticosteroids use of the patient. Type I cytokine (IFN-γ), IL-8, and IL-19 were associated with increased expression, while Type II cytokines (IL-4 and IL-13) with lower expression of ACE2 in lung tissue (airway epithelium and/or lung biopsies) of moderate and severe asthmatic patients. Of note, IL-19 was associated with ACE2 expression while IL-17 was associated with TMPRSS2 expression in sputum of asthmatic subjects. In vitro treatment of bronchial fibroblasts with IL-17 and IL-19 cytokines confirmed the regulatory effect of these cytokines on SARS-CoV-2 entry receptors. Our results suggest that the type of inflammation may regulate ACE2 and TMPRSS2 expression in the lung tissue of asthmatics and may hence affect susceptibility to SARS-CoV-2 infection. It is still controversial whether chronic lung inflammation increases the risk for COVID-19. One of the risk factors for acquiring COVID-19 is the level of expression of SARS-CoV-2 entry receptors, ACE2 and TMPRSS2, in lung tissue. It is, however, not clear how lung tissue inflammation affects expression levels of these receptors. We hence aimed to determine the level of SARS-CoV-2 receptors in lung tissue of asthmatic relative to age, gender, and asthma severity, and to investigate the factors regulating that. Therefore, gene expression data sets of well-known asthmatic cohorts (SARP and U-BIOPRED) were used to evaluate the association of ACE2 and TMPRSS2 with age, gender of the asthmatic patients, and also the type of the underlying lung tissue inflammatory cytokines. Notably, ACE2 and to less extent TMPRSS2 expression were upregulated in the lung tissue of asthmatics compared to healthy controls. Although a differential expression of ACE2, but not TMPRSS2 was observed relative to age within the moderate and severe asthma groups, our data suggest that age may not be a key regulatory factor of its expression. The type of tissue inflammation, however, associated significantly with ACE2 and TMPRSS2 expression levels following adjusting with age, gender and oral corticosteroids use of the patient. Type I cytokine (IFN-γ), IL-8, and IL-19 were associated with increased expression, while Type II cytokines (IL-4 and IL-13) with lower expression of ACE2 in lung tissue (airway epithelium and/or lung biopsies) of moderate and severe asthmatic patients. Of note, IL-19 was associated with ACE2 expression while IL-17 was associated with TMPRSS2 expression in sputum of asthmatic subjects. In vitro treatment of bronchial fibroblasts with IL-17 and IL-19 cytokines confirmed the regulatory effect of these cytokines on SARS-CoV-2 entry receptors. Our results suggest that the type of inflammation may regulate ACE2 and TMPRSS2 expression in the lung tissue of asthmatics and may hence affect susceptibility to SARS-CoV-2 infection. It is still controversial whether chronic lung inflammation increases the risk for COVID-19. One of the risk factors for acquiring COVID-19 is the level of expression of SARS-CoV-2 entry receptors, ACE2 and TMPRSS2, in lung tissue. It is, however, not clear how lung tissue inflammation affects expression levels of these receptors. We hence aimed to determine the level of SARS-CoV-2 receptors in lung tissue of asthmatic relative to age, gender, and asthma severity, and to investigate the factors regulating that. Therefore, gene expression data sets of well-known asthmatic cohorts (SARP and U-BIOPRED) were used to evaluate the association of ACE2 and TMPRSS2 with age, gender of the asthmatic patients, and also the type of the underlying lung tissue inflammatory cytokines. Notably, ACE2 and to less extent TMPRSS2 expression were upregulated in the lung tissue of asthmatics compared to healthy controls. Although a differential expression of ACE2, but not TMPRSS2 was observed relative to age within the moderate and severe asthma groups, our data suggest that age may not be a key regulatory factor of its expression. The type of tissue inflammation, however, associated significantly with ACE2 and TMPRSS2 expression levels following adjusting with age, gender and oral corticosteroids use of the patient. Type I cytokine (IFN-γ), IL-8, and IL-19 were associated with increased expression, while Type II cytokines (IL-4 and IL-13) with lower expression of ACE2 in lung tissue (airway epithelium and/or lung biopsies) of moderate and severe asthmatic patients. Of note, IL-19 was associated with ACE2 expression while IL-17 was associated with TMPRSS2 expression in sputum of asthmatic subjects. treatment of bronchial fibroblasts with IL-17 and IL-19 cytokines confirmed the regulatory effect of these cytokines on SARS-CoV-2 entry receptors. Our results suggest that the type of inflammation may regulate ACE2 and TMPRSS2 expression in the lung tissue of asthmatics and may hence affect susceptibility to SARS-CoV-2 infection. |
| Author | Saheb Sharif-Askari, Fatemeh Abdelrazig, Mawada Hamid, Qutayba Saheb Sharif-Askari, Narjes Al-Muhsen, Saleh Al Heialy, Saba Ratemi, Elaref Goel, Swati Hachim, Mahmood Yaseen Mahboub, Bassam Elzain, Eman Ibrahim Al-Hajjaj, Mohamed S. Hachim, Ibrahim Yaseen Salameh, Laila Halwani, Rabih Hafezi, Shirin |
| AuthorAffiliation | 2 College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences , Dubai , United Arab Emirates 1 Sharjah Institute of Medical Research, College of Medicine, University of Sharjah , Sharjah , United Arab Emirates 6 Immunology Research Lab, Department of Pediatrics, College of Medicine, King Saud University , Riyadh , Saudi Arabia 3 Meakins-Christie Laboratories, McGill University , Montreal, QC , Canada 9 Prince Abdullah Ben Khaled Celiac Disease Chair, department of pediatrics, Faculty of Medicine, King Saud University , Riyadh , Saudi Arabia 8 Jubail-Industrial College, Department of Chemical and Process Engineering Technology , Jubail-Industrial City , Saudi Arabia 4 Department of Clinical Sciences, College of Medicine, University of Sharjah , Sharjah , United Arab Emirates 5 Rashid Hospital, Dubai Health Authority , Dubai , United Arab Emirates 7 Department of Pediatrics, College of Medicine, King Saud University , Riyadh , Saudi Arabia |
| AuthorAffiliation_xml | – name: 1 Sharjah Institute of Medical Research, College of Medicine, University of Sharjah , Sharjah , United Arab Emirates – name: 2 College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences , Dubai , United Arab Emirates – name: 5 Rashid Hospital, Dubai Health Authority , Dubai , United Arab Emirates – name: 3 Meakins-Christie Laboratories, McGill University , Montreal, QC , Canada – name: 7 Department of Pediatrics, College of Medicine, King Saud University , Riyadh , Saudi Arabia – name: 9 Prince Abdullah Ben Khaled Celiac Disease Chair, department of pediatrics, Faculty of Medicine, King Saud University , Riyadh , Saudi Arabia – name: 6 Immunology Research Lab, Department of Pediatrics, College of Medicine, King Saud University , Riyadh , Saudi Arabia – name: 4 Department of Clinical Sciences, College of Medicine, University of Sharjah , Sharjah , United Arab Emirates – name: 8 Jubail-Industrial College, Department of Chemical and Process Engineering Technology , Jubail-Industrial City , Saudi Arabia |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35111161$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_arbres_2022_03_011 crossref_primary_10_1016_j_puhe_2024_02_031 crossref_primary_10_3389_fped_2024_1305639 crossref_primary_10_1016_j_jaci_2023_09_005 crossref_primary_10_1186_s12575_022_00177_9 crossref_primary_10_1002_ppul_26298 crossref_primary_10_1038_s41598_022_20087_w |
| Cites_doi | 10.3109/02770903.2016.1158268 10.1016/j.jaci.2020.04.009 10.1164/rccm.200907-1035OC 10.1183/23120541.00984-2020 10.3389/fimmu.2019.00968 10.1172/JCI36130 10.1038/nrg1297 10.1016/j.jaci.2008.04.016 10.1016/j.jaci.2020.05.004 10.1164/rccm.v202erratum7 10.1172/JCI64896 10.2202/1544-6115.1027 10.1378/chest.07-1881 10.1016/S0140-6736(20)30211-7 10.1186/gb-2014-15-2-r29 10.1016/j.biopha.2019.109193 10.1038/s41586-020-2521-4 10.1016/j.jaci.2020.07.026 10.1038/mi.2014.6 10.1186/1939-4551-7-8 10.1002/med.21756 10.1016/j.cell.2020.02.052 10.1155/2009/890349 10.1513/AnnalsATS.202006-613RL 10.1183/13993003.01805-2019 10.1165/ajrcmb.17.3.2733 10.1001/jama.2020.2648 10.1007/s12016-018-8712-1 10.1093/nar/gkv229 10.1128/JVI.00985-20 10.1126/sciimmunol.abc5367 10.4049/jimmunol.173.11.6712 10.1016/j.cell.2020.04.035 10.1002/alr.22672 |
| ContentType | Journal Article |
| Copyright | Copyright © 2022 Saheb Sharif-Askari, Goel, Saheb Sharif-Askari, Hafezi, Al Heialy, Hachim, Hachim, Mahboub, Salameh, Abdelrazig, Elzain, Al-Muhsen, Al-Hajjaj, Ratemi, Hamid and Halwani. Copyright © 2022 Saheb Sharif-Askari, Goel, Saheb Sharif-Askari, Hafezi, Al Heialy, Hachim, Hachim, Mahboub, Salameh, Abdelrazig, Elzain, Al-Muhsen, Al-Hajjaj, Ratemi, Hamid and Halwani 2022 Saheb Sharif-Askari, Goel, Saheb Sharif-Askari, Hafezi, Al Heialy, Hachim, Hachim, Mahboub, Salameh, Abdelrazig, Elzain, Al-Muhsen, Al-Hajjaj, Ratemi, Hamid and Halwani |
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| Keywords | COVID-19 ACE2 SARS-CoV-2 IL-19 IL-17 TMPRSS2 asthma cytokines |
| Language | English |
| License | Copyright © 2022 Saheb Sharif-Askari, Goel, Saheb Sharif-Askari, Hafezi, Al Heialy, Hachim, Hachim, Mahboub, Salameh, Abdelrazig, Elzain, Al-Muhsen, Al-Hajjaj, Ratemi, Hamid and Halwani. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Remo Castro Russo, Federal University of Minas Gerais, Brazil Reviewed by: Georgina Xanthou, Biomedical Research Foundation of the Academy of Athens (BRFAA), Greece; Priscilla Christina Olsen, Federal University of Rio de Janeiro, Brazil This article was submitted to Cytokines and Soluble Mediators in Immunity, a section of the journal Frontiers in Immunology |
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| SubjectTerms | ACE2 Adult Angiotensin-Converting Enzyme 2 - immunology asthma Asthma - immunology COVID-19 COVID-19 - immunology cytokines Cytokines - immunology Female Gene Expression Regulation - immunology Humans Immunology Lung - immunology Male Middle Aged SARS-CoV-2 SARS-CoV-2 - immunology Serine Endopeptidases - immunology TMPRSS2 |
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| Title | Asthma Associated Cytokines Regulate the Expression of SARS-CoV-2 Receptor ACE2 in the Lung Tissue of Asthmatic Patients |
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