SARS-CoV-2 activates the TLR4/MyD88 pathway in human macrophages: A possible correlation with strong pro-inflammatory responses in severe COVID-19
Toll-like receptors (TLRs) play a pivotal role in the immunologic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exaggerated inflammatory response of innate immune cells, however, may drive morbidity and death in Coronavirus disease 19 (COVID-19). We investigated...
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| Vydáno v: | Heliyon Ročník 9; číslo 11; s. e21893 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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England
Elsevier Ltd
01.11.2023
Elsevier |
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| ISSN: | 2405-8440, 2405-8440 |
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| Abstract | Toll-like receptors (TLRs) play a pivotal role in the immunologic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exaggerated inflammatory response of innate immune cells, however, may drive morbidity and death in Coronavirus disease 19 (COVID-19).
We investigated the engagement of SARS-CoV-2 with TLR4 in order to better understand how to tackle hyperinflammation in COVID-19.
We combined RNA-sequencing data of human lung tissue and of bronchoalveolar lavage fluid cells derived from COVID-19 patients with functional studies in human macrophages using SARS-CoV-2 spike proteins and viable SARS-CoV-2. Pharmacological inhibitors as well as gene editing with CRISPR/Cas9 were used to delineate the signalling pathways involved.
We found TLR4 to be the most abundantly upregulated TLR in human lung tissue irrespective of the underlying pathology. Accordingly, bronchoalveolar lavage fluid cells from patients with severe COVID-19 showed an NF-κB-pathway dominated immune response, whereas they were mostly defined by type I interferon signalling in moderate COVID-19. Mechanistically, we found the Spike ectodomain, but not receptor binding domain monomer to induce TLR4-dependent inflammation in human macrophages. By using pharmacological inhibitors as well as CRISPR/Cas9 deleted macrophages, we identify SARS-CoV-2 to engage canonical TLR4-MyD88 signalling. Importantly, we demonstrate that TLR4 blockage prevents exaggerated inflammatory responses in human macrophages infected with different SARS-CoV-2 variants, including immune escape variants B.1.1.7.-E484K and B.1.1.529 (omicron).
Our study critically extends the current knowledge on TLR-mediated hyperinflammatory responses to SARS-CoV-2 in human macrophages, paving the way for novel approaches to tackle severe COVID-19.
Our study combining human lung transcriptomics with functional studies in human macrophages clearly supports the design and development of TLR4 - directed therapeutics to mitigate hyperinflammation in severe COVID-19.
•TLR4 is the most abundantly upregulated TLR in human lung irrespective of the underlying pathology.•BALF MΦ from patients with severe COVID-19 show strong upregulation of the NF-κB pathway.•The ectodomain of the SARS-COV-2 spike protein leads to TLR4 dependent upregulation of IL-6.•Viable SARS-CoV-2 leads to TLR4 dependent IL-6 upregulation irrespective of the variant of concern.•TLR4 inhibition in SARS-CoV-2 infected MΦ leads to downregulation of genes involved in leukocyte migration. |
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| AbstractList | Toll-like receptors (TLRs) play a pivotal role in the immunologic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exaggerated inflammatory response of innate immune cells, however, may drive morbidity and death in Coronavirus disease 19 (COVID-19).
We investigated the engagement of SARS-CoV-2 with TLR4 in order to better understand how to tackle hyperinflammation in COVID-19.
We combined RNA-sequencing data of human lung tissue and of bronchoalveolar lavage fluid cells derived from COVID-19 patients with functional studies in human macrophages using SARS-CoV-2 spike proteins and viable SARS-CoV-2. Pharmacological inhibitors as well as gene editing with CRISPR/Cas9 were used to delineate the signalling pathways involved.
We found TLR4 to be the most abundantly upregulated TLR in human lung tissue irrespective of the underlying pathology. Accordingly, bronchoalveolar lavage fluid cells from patients with severe COVID-19 showed an NF-κB-pathway dominated immune response, whereas they were mostly defined by type I interferon signalling in moderate COVID-19. Mechanistically, we found the Spike ectodomain, but not receptor binding domain monomer to induce TLR4-dependent inflammation in human macrophages. By using pharmacological inhibitors as well as CRISPR/Cas9 deleted macrophages, we identify SARS-CoV-2 to engage canonical TLR4-MyD88 signalling. Importantly, we demonstrate that TLR4 blockage prevents exaggerated inflammatory responses in human macrophages infected with different SARS-CoV-2 variants, including immune escape variants B.1.1.7.-E484K and B.1.1.529 (omicron).
Our study critically extends the current knowledge on TLR-mediated hyperinflammatory responses to SARS-CoV-2 in human macrophages, paving the way for novel approaches to tackle severe COVID-19.
Our study combining human lung transcriptomics with functional studies in human macrophages clearly supports the design and development of TLR4 - directed therapeutics to mitigate hyperinflammation in severe COVID-19. Background: Toll-like receptors (TLRs) play a pivotal role in the immunologic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exaggerated inflammatory response of innate immune cells, however, may drive morbidity and death in Coronavirus disease 19 (COVID-19). Objective: We investigated the engagement of SARS-CoV-2 with TLR4 in order to better understand how to tackle hyperinflammation in COVID-19. Methods: We combined RNA-sequencing data of human lung tissue and of bronchoalveolar lavage fluid cells derived from COVID-19 patients with functional studies in human macrophages using SARS-CoV-2 spike proteins and viable SARS-CoV-2. Pharmacological inhibitors as well as gene editing with CRISPR/Cas9 were used to delineate the signalling pathways involved. Results: We found TLR4 to be the most abundantly upregulated TLR in human lung tissue irrespective of the underlying pathology. Accordingly, bronchoalveolar lavage fluid cells from patients with severe COVID-19 showed an NF-κB-pathway dominated immune response, whereas they were mostly defined by type I interferon signalling in moderate COVID-19. Mechanistically, we found the Spike ectodomain, but not receptor binding domain monomer to induce TLR4-dependent inflammation in human macrophages. By using pharmacological inhibitors as well as CRISPR/Cas9 deleted macrophages, we identify SARS-CoV-2 to engage canonical TLR4-MyD88 signalling. Importantly, we demonstrate that TLR4 blockage prevents exaggerated inflammatory responses in human macrophages infected with different SARS-CoV-2 variants, including immune escape variants B.1.1.7.-E484K and B.1.1.529 (omicron). Conclusion: Our study critically extends the current knowledge on TLR-mediated hyperinflammatory responses to SARS-CoV-2 in human macrophages, paving the way for novel approaches to tackle severe COVID-19. Take-home message: Our study combining human lung transcriptomics with functional studies in human macrophages clearly supports the design and development of TLR4 - directed therapeutics to mitigate hyperinflammation in severe COVID-19. Toll-like receptors (TLRs) play a pivotal role in the immunologic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exaggerated inflammatory response of innate immune cells, however, may drive morbidity and death in Coronavirus disease 19 (COVID-19).BackgroundToll-like receptors (TLRs) play a pivotal role in the immunologic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exaggerated inflammatory response of innate immune cells, however, may drive morbidity and death in Coronavirus disease 19 (COVID-19).We investigated the engagement of SARS-CoV-2 with TLR4 in order to better understand how to tackle hyperinflammation in COVID-19.ObjectiveWe investigated the engagement of SARS-CoV-2 with TLR4 in order to better understand how to tackle hyperinflammation in COVID-19.We combined RNA-sequencing data of human lung tissue and of bronchoalveolar lavage fluid cells derived from COVID-19 patients with functional studies in human macrophages using SARS-CoV-2 spike proteins and viable SARS-CoV-2. Pharmacological inhibitors as well as gene editing with CRISPR/Cas9 were used to delineate the signalling pathways involved.MethodsWe combined RNA-sequencing data of human lung tissue and of bronchoalveolar lavage fluid cells derived from COVID-19 patients with functional studies in human macrophages using SARS-CoV-2 spike proteins and viable SARS-CoV-2. Pharmacological inhibitors as well as gene editing with CRISPR/Cas9 were used to delineate the signalling pathways involved.We found TLR4 to be the most abundantly upregulated TLR in human lung tissue irrespective of the underlying pathology. Accordingly, bronchoalveolar lavage fluid cells from patients with severe COVID-19 showed an NF-κB-pathway dominated immune response, whereas they were mostly defined by type I interferon signalling in moderate COVID-19. Mechanistically, we found the Spike ectodomain, but not receptor binding domain monomer to induce TLR4-dependent inflammation in human macrophages. By using pharmacological inhibitors as well as CRISPR/Cas9 deleted macrophages, we identify SARS-CoV-2 to engage canonical TLR4-MyD88 signalling. Importantly, we demonstrate that TLR4 blockage prevents exaggerated inflammatory responses in human macrophages infected with different SARS-CoV-2 variants, including immune escape variants B.1.1.7.-E484K and B.1.1.529 (omicron).ResultsWe found TLR4 to be the most abundantly upregulated TLR in human lung tissue irrespective of the underlying pathology. Accordingly, bronchoalveolar lavage fluid cells from patients with severe COVID-19 showed an NF-κB-pathway dominated immune response, whereas they were mostly defined by type I interferon signalling in moderate COVID-19. Mechanistically, we found the Spike ectodomain, but not receptor binding domain monomer to induce TLR4-dependent inflammation in human macrophages. By using pharmacological inhibitors as well as CRISPR/Cas9 deleted macrophages, we identify SARS-CoV-2 to engage canonical TLR4-MyD88 signalling. Importantly, we demonstrate that TLR4 blockage prevents exaggerated inflammatory responses in human macrophages infected with different SARS-CoV-2 variants, including immune escape variants B.1.1.7.-E484K and B.1.1.529 (omicron).Our study critically extends the current knowledge on TLR-mediated hyperinflammatory responses to SARS-CoV-2 in human macrophages, paving the way for novel approaches to tackle severe COVID-19.ConclusionOur study critically extends the current knowledge on TLR-mediated hyperinflammatory responses to SARS-CoV-2 in human macrophages, paving the way for novel approaches to tackle severe COVID-19.Our study combining human lung transcriptomics with functional studies in human macrophages clearly supports the design and development of TLR4 - directed therapeutics to mitigate hyperinflammation in severe COVID-19.Take-home messageOur study combining human lung transcriptomics with functional studies in human macrophages clearly supports the design and development of TLR4 - directed therapeutics to mitigate hyperinflammation in severe COVID-19. • TLR4 is the most abundantly upregulated TLR in human lung irrespective of the underlying pathology. • BALF MΦ from patients with severe COVID-19 show strong upregulation of the NF-κB pathway. • The ectodomain of the SARS-COV-2 spike protein leads to TLR4 dependent upregulation of IL-6. • Viable SARS-CoV-2 leads to TLR4 dependent IL-6 upregulation irrespective of the variant of concern. • TLR4 inhibition in SARS-CoV-2 infected MΦ leads to downregulation of genes involved in leukocyte migration. Toll-like receptors (TLRs) play a pivotal role in the immunologic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exaggerated inflammatory response of innate immune cells, however, may drive morbidity and death in Coronavirus disease 19 (COVID-19). We investigated the engagement of SARS-CoV-2 with TLR4 in order to better understand how to tackle hyperinflammation in COVID-19. We combined RNA-sequencing data of human lung tissue and of bronchoalveolar lavage fluid cells derived from COVID-19 patients with functional studies in human macrophages using SARS-CoV-2 spike proteins and viable SARS-CoV-2. Pharmacological inhibitors as well as gene editing with CRISPR/Cas9 were used to delineate the signalling pathways involved. We found TLR4 to be the most abundantly upregulated TLR in human lung tissue irrespective of the underlying pathology. Accordingly, bronchoalveolar lavage fluid cells from patients with severe COVID-19 showed an NF-κB-pathway dominated immune response, whereas they were mostly defined by type I interferon signalling in moderate COVID-19. Mechanistically, we found the Spike ectodomain, but not receptor binding domain monomer to induce TLR4-dependent inflammation in human macrophages. By using pharmacological inhibitors as well as CRISPR/Cas9 deleted macrophages, we identify SARS-CoV-2 to engage canonical TLR4-MyD88 signalling. Importantly, we demonstrate that TLR4 blockage prevents exaggerated inflammatory responses in human macrophages infected with different SARS-CoV-2 variants, including immune escape variants B.1.1.7.-E484K and B.1.1.529 (omicron). Our study critically extends the current knowledge on TLR-mediated hyperinflammatory responses to SARS-CoV-2 in human macrophages, paving the way for novel approaches to tackle severe COVID-19. Our study combining human lung transcriptomics with functional studies in human macrophages clearly supports the design and development of TLR4 - directed therapeutics to mitigate hyperinflammation in severe COVID-19. Toll-like receptors (TLRs) play a pivotal role in the immunologic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exaggerated inflammatory response of innate immune cells, however, may drive morbidity and death in Coronavirus disease 19 (COVID-19). We investigated the engagement of SARS-CoV-2 with TLR4 in order to better understand how to tackle hyperinflammation in COVID-19. We combined RNA-sequencing data of human lung tissue and of bronchoalveolar lavage fluid cells derived from COVID-19 patients with functional studies in human macrophages using SARS-CoV-2 spike proteins and viable SARS-CoV-2. Pharmacological inhibitors as well as gene editing with CRISPR/Cas9 were used to delineate the signalling pathways involved. We found TLR4 to be the most abundantly upregulated TLR in human lung tissue irrespective of the underlying pathology. Accordingly, bronchoalveolar lavage fluid cells from patients with severe COVID-19 showed an NF-κB-pathway dominated immune response, whereas they were mostly defined by type I interferon signalling in moderate COVID-19. Mechanistically, we found the Spike ectodomain, but not receptor binding domain monomer to induce TLR4-dependent inflammation in human macrophages. By using pharmacological inhibitors as well as CRISPR/Cas9 deleted macrophages, we identify SARS-CoV-2 to engage canonical TLR4-MyD88 signalling. Importantly, we demonstrate that TLR4 blockage prevents exaggerated inflammatory responses in human macrophages infected with different SARS-CoV-2 variants, including immune escape variants B.1.1.7.-E484K and B.1.1.529 (omicron). Our study critically extends the current knowledge on TLR-mediated hyperinflammatory responses to SARS-CoV-2 in human macrophages, paving the way for novel approaches to tackle severe COVID-19. Our study combining human lung transcriptomics with functional studies in human macrophages clearly supports the design and development of TLR4 - directed therapeutics to mitigate hyperinflammation in severe COVID-19. •TLR4 is the most abundantly upregulated TLR in human lung irrespective of the underlying pathology.•BALF MΦ from patients with severe COVID-19 show strong upregulation of the NF-κB pathway.•The ectodomain of the SARS-COV-2 spike protein leads to TLR4 dependent upregulation of IL-6.•Viable SARS-CoV-2 leads to TLR4 dependent IL-6 upregulation irrespective of the variant of concern.•TLR4 inhibition in SARS-CoV-2 infected MΦ leads to downregulation of genes involved in leukocyte migration. |
| ArticleNumber | e21893 |
| Author | Zinner, Carl P. Hirsch, Jakob Dünser, Christina Yurchenko, Maria Tancevski, Ivan Weiss, Guenter Lener, Daniela Tzankov, Alexandar Rieder, Dietmar Holfeld, Johannes Löffler-Ragg, Judith Fischer, Christine Gollmann-Tepeköylü, Can Schirmer, Michael Theurl, Markus Wilflingseder, Doris Zhang, Shen-Ying Sahanic, Sabina Krogsdam, Anne Tymoszuk, Piotr Casanova, Jean-Laurent Hilbe, Richard Posch, Wilfried Trajanoski, Zlatko Demetz, Egon |
| Author_xml | – sequence: 1 givenname: Sabina surname: Sahanic fullname: Sahanic, Sabina organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 2 givenname: Richard surname: Hilbe fullname: Hilbe, Richard organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 3 givenname: Christina surname: Dünser fullname: Dünser, Christina organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 4 givenname: Piotr orcidid: 0000-0002-0398-6034 surname: Tymoszuk fullname: Tymoszuk, Piotr organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 5 givenname: Judith surname: Löffler-Ragg fullname: Löffler-Ragg, Judith organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 6 givenname: Dietmar surname: Rieder fullname: Rieder, Dietmar organization: Institute of Bioinformatics, Biocenter, Medical University of Innsbruck, Innsbruck, Austria – sequence: 7 givenname: Zlatko surname: Trajanoski fullname: Trajanoski, Zlatko organization: Institute of Bioinformatics, Biocenter, Medical University of Innsbruck, Innsbruck, Austria – sequence: 8 givenname: Anne orcidid: 0000-0002-5478-0511 surname: Krogsdam fullname: Krogsdam, Anne organization: Institute of Bioinformatics, Biocenter, Medical University of Innsbruck, Innsbruck, Austria – sequence: 9 givenname: Egon surname: Demetz fullname: Demetz, Egon organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 10 givenname: Maria orcidid: 0000-0002-0516-4747 surname: Yurchenko fullname: Yurchenko, Maria organization: Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway – sequence: 11 givenname: Christine orcidid: 0000-0002-5656-5030 surname: Fischer fullname: Fischer, Christine organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 12 givenname: Michael orcidid: 0000-0001-9208-7809 surname: Schirmer fullname: Schirmer, Michael organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 13 givenname: Markus orcidid: 0000-0002-3609-9730 surname: Theurl fullname: Theurl, Markus organization: Department of Internal Medicine III, Medical University of Innsbruck, Innsbruck, Austria – sequence: 14 givenname: Daniela orcidid: 0000-0002-3464-0343 surname: Lener fullname: Lener, Daniela organization: Department of Internal Medicine III, Medical University of Innsbruck, Innsbruck, Austria – sequence: 15 givenname: Jakob surname: Hirsch fullname: Hirsch, Jakob organization: Department of Cardiac Surgery, Medical University of Innsbruck, Innsbruck, Austria – sequence: 16 givenname: Johannes surname: Holfeld fullname: Holfeld, Johannes organization: Department of Cardiac Surgery, Medical University of Innsbruck, Innsbruck, Austria – sequence: 17 givenname: Can surname: Gollmann-Tepeköylü fullname: Gollmann-Tepeköylü, Can organization: Department of Cardiac Surgery, Medical University of Innsbruck, Innsbruck, Austria – sequence: 18 givenname: Carl P. surname: Zinner fullname: Zinner, Carl P. organization: Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Switzerland – sequence: 19 givenname: Alexandar orcidid: 0000-0002-1100-3819 surname: Tzankov fullname: Tzankov, Alexandar organization: Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Switzerland – sequence: 20 givenname: Shen-Ying surname: Zhang fullname: Zhang, Shen-Ying organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France – sequence: 21 givenname: Jean-Laurent surname: Casanova fullname: Casanova, Jean-Laurent organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France – sequence: 22 givenname: Wilfried surname: Posch fullname: Posch, Wilfried email: wilfried.posch@i-med.ac.at organization: Division of Hygiene and Medical Microbiology, Medical University of Innsbruck, Austria – sequence: 23 givenname: Doris orcidid: 0000-0002-5888-5118 surname: Wilflingseder fullname: Wilflingseder, Doris email: doris.wilflingseder@i-med.ac.at organization: Division of Hygiene and Medical Microbiology, Medical University of Innsbruck, Austria – sequence: 24 givenname: Guenter surname: Weiss fullname: Weiss, Guenter organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria – sequence: 25 givenname: Ivan surname: Tancevski fullname: Tancevski, Ivan email: ivan.tancevski@i-med.ac.at organization: Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38034686$$D View this record in MEDLINE/PubMed |
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| Keywords | COVID-19 Toll-like receptors Innate immunity SARS-CoV-2 Macrophages |
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| SubjectTerms | COVID-19 COVID-19 infection CRISPR-Cas systems death domain genes humans immune response inflammation Innate immunity interferons lungs Macrophages morbidity SARS-CoV-2 sequence analysis Severe acute respiratory syndrome coronavirus 2 therapeutics Toll-like receptors transcriptomics |
| Title | SARS-CoV-2 activates the TLR4/MyD88 pathway in human macrophages: A possible correlation with strong pro-inflammatory responses in severe COVID-19 |
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