Imiquimod Boosts Interferon Response, and Decreases ACE2 and Pro-Inflammatory Response of Human Bronchial Epithelium in Asthma
Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity. To investigate bronch...
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Published in | Frontiers in immunology Vol. 12; p. 743890 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
07.12.2021
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Online Access | Get full text |
ISSN | 1664-3224 1664-3224 |
DOI | 10.3389/fimmu.2021.743890 |
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Abstract | Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in
cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity.
To investigate bronchial epithelial effects of imiquimod of potential importance for anti-viral treatment in asthmatic patients.
Effects of imiquimod alone were examined in HBECs from healthy (N=4) and asthmatic (N=18) donors. Mimicking SARS-CoV-2 infection, HBECs were stimulated with poly(I:C), a dsRNA analogue, or SARS-CoV-2 spike-protein 1 (SP1; receptor binding) with and without imiquimod treatment. Expression of SARS-CoV-2 receptor (ACE2), pro-inflammatory and anti-viral cytokines were analyzed by RT-qPCR, multiplex ELISA, western blot, and Nanostring and proteomic analyses.
Imiquimod reduced ACE2 expression at baseline and after poly(I:C) stimulation. Imiquimod also reduced poly(I:C)-induced pro-inflammatory cytokines including IL-1β, IL-6, IL-8, and IL-33. Furthermore, imiquimod increased IFN-β expression, an effect potentiated in presence of poly(I:C) or SP1. Multiplex mRNA analysis verified enrichment in type-I IFN signaling concomitant with suppression of cytokine signaling pathways induced by imiquimod in presence of poly(I:C). Exploratory proteomic analyses revealed potentially protective effects of imiquimod on infections.
Imiquimod triggers viral resistance mechanisms in HBECs by decreasing ACE2 and increasing IFN-β expression. Additionally, imiquimod improves viral infection tolerance by reducing viral stimulus-induced epithelial cytokines involved in severe COVID-19 infection. Our imiquimod data highlight feasibility of producing pluripotent drugs potentially suited for anti-viral treatment in asthmatic subjects. |
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AbstractList | Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in
cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity.
To investigate bronchial epithelial effects of imiquimod of potential importance for anti-viral treatment in asthmatic patients.
Effects of imiquimod alone were examined in HBECs from healthy (N=4) and asthmatic (N=18) donors. Mimicking SARS-CoV-2 infection, HBECs were stimulated with poly(I:C), a dsRNA analogue, or SARS-CoV-2 spike-protein 1 (SP1; receptor binding) with and without imiquimod treatment. Expression of SARS-CoV-2 receptor (ACE2), pro-inflammatory and anti-viral cytokines were analyzed by RT-qPCR, multiplex ELISA, western blot, and Nanostring and proteomic analyses.
Imiquimod reduced ACE2 expression at baseline and after poly(I:C) stimulation. Imiquimod also reduced poly(I:C)-induced pro-inflammatory cytokines including IL-1β, IL-6, IL-8, and IL-33. Furthermore, imiquimod increased IFN-β expression, an effect potentiated in presence of poly(I:C) or SP1. Multiplex mRNA analysis verified enrichment in type-I IFN signaling concomitant with suppression of cytokine signaling pathways induced by imiquimod in presence of poly(I:C). Exploratory proteomic analyses revealed potentially protective effects of imiquimod on infections.
Imiquimod triggers viral resistance mechanisms in HBECs by decreasing ACE2 and increasing IFN-β expression. Additionally, imiquimod improves viral infection tolerance by reducing viral stimulus-induced epithelial cytokines involved in severe COVID-19 infection. Our imiquimod data highlight feasibility of producing pluripotent drugs potentially suited for anti-viral treatment in asthmatic subjects. BackgroundBoth anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in ex vivo cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity.ObjectiveTo investigate bronchial epithelial effects of imiquimod of potential importance for anti-viral treatment in asthmatic patients.MethodsEffects of imiquimod alone were examined in HBECs from healthy (N=4) and asthmatic (N=18) donors. Mimicking SARS-CoV-2 infection, HBECs were stimulated with poly(I:C), a dsRNA analogue, or SARS-CoV-2 spike-protein 1 (SP1; receptor binding) with and without imiquimod treatment. Expression of SARS-CoV-2 receptor (ACE2), pro-inflammatory and anti-viral cytokines were analyzed by RT-qPCR, multiplex ELISA, western blot, and Nanostring and proteomic analyses.ResultsImiquimod reduced ACE2 expression at baseline and after poly(I:C) stimulation. Imiquimod also reduced poly(I:C)-induced pro-inflammatory cytokines including IL-1β, IL-6, IL-8, and IL-33. Furthermore, imiquimod increased IFN-β expression, an effect potentiated in presence of poly(I:C) or SP1. Multiplex mRNA analysis verified enrichment in type-I IFN signaling concomitant with suppression of cytokine signaling pathways induced by imiquimod in presence of poly(I:C). Exploratory proteomic analyses revealed potentially protective effects of imiquimod on infections.ConclusionImiquimod triggers viral resistance mechanisms in HBECs by decreasing ACE2 and increasing IFN-β expression. Additionally, imiquimod improves viral infection tolerance by reducing viral stimulus-induced epithelial cytokines involved in severe COVID-19 infection. Our imiquimod data highlight feasibility of producing pluripotent drugs potentially suited for anti-viral treatment in asthmatic subjects. Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in ex vivo cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity.BackgroundBoth anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in ex vivo cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity.To investigate bronchial epithelial effects of imiquimod of potential importance for anti-viral treatment in asthmatic patients.ObjectiveTo investigate bronchial epithelial effects of imiquimod of potential importance for anti-viral treatment in asthmatic patients.Effects of imiquimod alone were examined in HBECs from healthy (N=4) and asthmatic (N=18) donors. Mimicking SARS-CoV-2 infection, HBECs were stimulated with poly(I:C), a dsRNA analogue, or SARS-CoV-2 spike-protein 1 (SP1; receptor binding) with and without imiquimod treatment. Expression of SARS-CoV-2 receptor (ACE2), pro-inflammatory and anti-viral cytokines were analyzed by RT-qPCR, multiplex ELISA, western blot, and Nanostring and proteomic analyses.MethodsEffects of imiquimod alone were examined in HBECs from healthy (N=4) and asthmatic (N=18) donors. Mimicking SARS-CoV-2 infection, HBECs were stimulated with poly(I:C), a dsRNA analogue, or SARS-CoV-2 spike-protein 1 (SP1; receptor binding) with and without imiquimod treatment. Expression of SARS-CoV-2 receptor (ACE2), pro-inflammatory and anti-viral cytokines were analyzed by RT-qPCR, multiplex ELISA, western blot, and Nanostring and proteomic analyses.Imiquimod reduced ACE2 expression at baseline and after poly(I:C) stimulation. Imiquimod also reduced poly(I:C)-induced pro-inflammatory cytokines including IL-1β, IL-6, IL-8, and IL-33. Furthermore, imiquimod increased IFN-β expression, an effect potentiated in presence of poly(I:C) or SP1. Multiplex mRNA analysis verified enrichment in type-I IFN signaling concomitant with suppression of cytokine signaling pathways induced by imiquimod in presence of poly(I:C). Exploratory proteomic analyses revealed potentially protective effects of imiquimod on infections.ResultsImiquimod reduced ACE2 expression at baseline and after poly(I:C) stimulation. Imiquimod also reduced poly(I:C)-induced pro-inflammatory cytokines including IL-1β, IL-6, IL-8, and IL-33. Furthermore, imiquimod increased IFN-β expression, an effect potentiated in presence of poly(I:C) or SP1. Multiplex mRNA analysis verified enrichment in type-I IFN signaling concomitant with suppression of cytokine signaling pathways induced by imiquimod in presence of poly(I:C). Exploratory proteomic analyses revealed potentially protective effects of imiquimod on infections.Imiquimod triggers viral resistance mechanisms in HBECs by decreasing ACE2 and increasing IFN-β expression. Additionally, imiquimod improves viral infection tolerance by reducing viral stimulus-induced epithelial cytokines involved in severe COVID-19 infection. Our imiquimod data highlight feasibility of producing pluripotent drugs potentially suited for anti-viral treatment in asthmatic subjects.ConclusionImiquimod triggers viral resistance mechanisms in HBECs by decreasing ACE2 and increasing IFN-β expression. Additionally, imiquimod improves viral infection tolerance by reducing viral stimulus-induced epithelial cytokines involved in severe COVID-19 infection. Our imiquimod data highlight feasibility of producing pluripotent drugs potentially suited for anti-viral treatment in asthmatic subjects. Background: Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in ex vivo cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity. Objective: To investigate bronchial epithelial effects of imiquimod of potential importance for anti-viral treatment in asthmatic patients. Methods: Effects of imiquimod alone were examined in HBECs from healthy (N=4) and asthmatic (N=18) donors. Mimicking SARS-CoV-2 infection, HBECs were stimulated with poly(I:C), a dsRNA analogue, or SARS-CoV-2 spike-protein 1 (SP1; receptor binding) with and without imiquimod treatment. Expression of SARS-CoV-2 receptor (ACE2), pro-inflammatory and anti-viral cytokines were analyzed by RT-qPCR, multiplex ELISA, western blot, and Nanostring and proteomic analyses. Results: Imiquimod reduced ACE2 expression at baseline and after poly(I:C) stimulation. Imiquimod also reduced poly(I:C)-induced pro-inflammatory cytokines including IL-1β, IL-6, IL-8, and IL-33. Furthermore, imiquimod increased IFN-β expression, an effect potentiated in presence of poly(I:C) or SP1. Multiplex mRNA analysis verified enrichment in type-I IFN signaling concomitant with suppression of cytokine signaling pathways induced by imiquimod in presence of poly(I:C). Exploratory proteomic analyses revealed potentially protective effects of imiquimod on infections. Conclusion: Imiquimod triggers viral resistance mechanisms in HBECs by decreasing ACE2 and increasing IFN-β expression. Additionally, imiquimod improves viral infection tolerance by reducing viral stimulus-induced epithelial cytokines involved in severe COVID-19 infection. Our imiquimod data highlight feasibility of producing pluripotent drugs potentially suited for anti-viral treatment in asthmatic subjects. |
Author | Sverrild, Asger Ramu, Sangeetha Uller, Lena Hvidtfeldt, Morten Porsbjerg, Celeste Nieto-Fontarigo, Juan José Menzel, Mandy Cerps, Samuel Sander, Adam Frederik Tillgren, Sofia |
AuthorAffiliation | 2 Department of Respiratory Medicine, University Hospital Bispebjerg , Copenhagen , Denmark 4 Department of Infectious Disease, Copenhagen University Hospital , Copenhagen , Denmark 1 Department of Experimental Medical Science, Lund University , Lund , Sweden 3 Department for Immunology and Microbiology, Faculty of Health and Medical Sciences, Centre for Medical Parasitology, University of Copenhagen , Copenhagen , Denmark |
AuthorAffiliation_xml | – name: 1 Department of Experimental Medical Science, Lund University , Lund , Sweden – name: 2 Department of Respiratory Medicine, University Hospital Bispebjerg , Copenhagen , Denmark – name: 4 Department of Infectious Disease, Copenhagen University Hospital , Copenhagen , Denmark – name: 3 Department for Immunology and Microbiology, Faculty of Health and Medical Sciences, Centre for Medical Parasitology, University of Copenhagen , Copenhagen , Denmark |
Author_xml | – sequence: 1 givenname: Juan José surname: Nieto-Fontarigo fullname: Nieto-Fontarigo, Juan José – sequence: 2 givenname: Sofia surname: Tillgren fullname: Tillgren, Sofia – sequence: 3 givenname: Samuel surname: Cerps fullname: Cerps, Samuel – sequence: 4 givenname: Asger surname: Sverrild fullname: Sverrild, Asger – sequence: 5 givenname: Morten surname: Hvidtfeldt fullname: Hvidtfeldt, Morten – sequence: 6 givenname: Sangeetha surname: Ramu fullname: Ramu, Sangeetha – sequence: 7 givenname: Mandy surname: Menzel fullname: Menzel, Mandy – sequence: 8 givenname: Adam Frederik surname: Sander fullname: Sander, Adam Frederik – sequence: 9 givenname: Celeste surname: Porsbjerg fullname: Porsbjerg, Celeste – sequence: 10 givenname: Lena surname: Uller fullname: Uller, Lena |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34950134$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_3389_fimmu_2023_1294434 crossref_primary_10_1007_s00011_022_01596_w crossref_primary_10_3390_microorganisms12102030 crossref_primary_10_1002_mco2_549 crossref_primary_10_3389_fimmu_2022_865973 crossref_primary_10_3390_ijms25147661 |
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Copyright | Copyright © 2021 Nieto-Fontarigo, Tillgren, Cerps, Sverrild, Hvidtfeldt, Ramu, Menzel, Sander, Porsbjerg and Uller. Copyright © 2021 Nieto-Fontarigo, Tillgren, Cerps, Sverrild, Hvidtfeldt, Ramu, Menzel, Sander, Porsbjerg and Uller 2021 Nieto-Fontarigo, Tillgren, Cerps, Sverrild, Hvidtfeldt, Ramu, Menzel, Sander, Porsbjerg and Uller |
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CorporateAuthor | Respiratory Immunopharmacology Department of Experimental Medical Science Faculty of Medicine Lunds universitet Institutionen för experimentell medicinsk vetenskap Medicinska fakulteten Lund University Respiratorisk immunofarmakologi |
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Keywords | COVID-19 SARS – CoV – 2 asthma anti-viral drug TLR7 agonist imiquimod |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Axel Lorentz, University of Hohenheim, Germany Reviewed by: Thomas A. Kufer, University of Hohenheim, Germany; Andrew Higham, The University of Manchester, United Kingdom This article was submitted to Molecular Innate Immunity, a section of the journal Frontiers in Immunology These authors have contributed equally to this work and share first authorship |
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Snippet | Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7... Background: Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a... BackgroundBoth anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a... |
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SubjectTerms | Adjuvants, Immunologic - pharmacology Adult Aged Angiotensin-Converting Enzyme 2 - metabolism anti-viral drug Asthma Basic Medicine Bronchi - drug effects Bronchi - immunology Bronchi - virology Cells, Cultured COVID-19 Female Humans imiquimod Imiquimod - pharmacology Immunologi inom det medicinska området (Här ingår: Cell- och immunterapi) Immunology Immunology in the Medical Area (including Cell and Immunotherapy) Interferon-beta - drug effects Interferon-beta - immunology Male Medical and Health Sciences Medicin och hälsovetenskap Medicinska och farmaceutiska grundvetenskaper Middle Aged Respiratory Mucosa - drug effects Respiratory Mucosa - metabolism Respiratory Mucosa - virology SARS – CoV – 2 TLR7 agonist |
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Title | Imiquimod Boosts Interferon Response, and Decreases ACE2 and Pro-Inflammatory Response of Human Bronchial Epithelium in Asthma |
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