TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase
Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in T...
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| Published in: | Nature communications Vol. 14; no. 1; pp. 7349 - 24 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
Nature Publishing Group UK
14.11.2023
Nature Publishing Group Nature Portfolio |
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| ISSN: | 2041-1723, 2041-1723 |
| Online Access: | Get full text |
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| Abstract | Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly,
TLR7
mRNA is increased in pre-existing datasets from patients with COPD, while TLR7
+
mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target.
Toll-like receptor 7 (TLR7) normally recognizes exogenous single-stranded RNA for the activation of innate immunity. Here the authors show that TLR7 may also contribute, via the modulation of mast cell functions, to experimental, cigarette smoke-induced mouse models of emphysema, thereby hinting TLR7 as a potential therapeutic target for human lung inflammation. |
|---|---|
| AbstractList | Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly,
TLR7
mRNA is increased in pre-existing datasets from patients with COPD, while TLR7
+
mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target.
Toll-like receptor 7 (TLR7) normally recognizes exogenous single-stranded RNA for the activation of innate immunity. Here the authors show that TLR7 may also contribute, via the modulation of mast cell functions, to experimental, cigarette smoke-induced mouse models of emphysema, thereby hinting TLR7 as a potential therapeutic target for human lung inflammation. Abstract Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly, TLR7 mRNA is increased in pre-existing datasets from patients with COPD, while TLR7+ mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target. Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly, TLR7 mRNA is increased in pre-existing datasets from patients with COPD, while TLR7+ mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target.Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly, TLR7 mRNA is increased in pre-existing datasets from patients with COPD, while TLR7+ mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target. Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly, TLR7 mRNA is increased in pre-existing datasets from patients with COPD, while TLR7 + mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target. Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly, TLR7 mRNA is increased in pre-existing datasets from patients with COPD, while TLR7 mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target. Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly, TLR7 mRNA is increased in pre-existing datasets from patients with COPD, while TLR7+ mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target.Toll-like receptor 7 (TLR7) normally recognizes exogenous single-stranded RNA for the activation of innate immunity. Here the authors show that TLR7 may also contribute, via the modulation of mast cell functions, to experimental, cigarette smoke-induced mouse models of emphysema, thereby hinting TLR7 as a potential therapeutic target for human lung inflammation. |
| ArticleNumber | 7349 |
| Author | Liu, Gang Fukui, Ryutaro Ieni, Antonio Idrees, Sobia Mattes, Joerg Chotirmall, Sanjay H. Adcock, Ian M. Philp, Ashleigh M. Murakami, Yusuke Tan, Nguan Soon Estepar, Raul San Jose Cheng, Hong Sheng Polverino, Francesca Collison, Adam M. Caramori, Gaetano Hansbro, Philip M. Hanish, Irwan Wark, Peter A. Kim, Richard Y. Sohal, Sukhwinder S. Pavlidis, Stelios Bracke, Ken R. Gomez, Henry M. Foster, Paul S. Starkey, Malcolm R. Nair, Prema M. Hortle, Elinor Miyake, Kensuke Rojas-Quintero, Joselyn Marshall, Jacqueline E. Horvat, Jay C. Pickles, Sophie Monaco, Francesco Haw, Tatt Jhong Oliver, Brian GG Sin, Don D. Hsu, Alan CY Faiz, Alen Nalkurthi, Christina Hansbro, Nicole G. |
| Author_xml | – sequence: 1 givenname: Gang orcidid: 0000-0002-0489-2638 surname: Liu fullname: Liu, Gang organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney – sequence: 2 givenname: Tatt Jhong orcidid: 0000-0003-2315-7089 surname: Haw fullname: Haw, Tatt Jhong organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 3 givenname: Malcolm R. surname: Starkey fullname: Starkey, Malcolm R. organization: Depatrment of Immunology and Pathology, Central Clinical School, Monash University – sequence: 4 givenname: Ashleigh M. surname: Philp fullname: Philp, Ashleigh M. organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney, School of Clinical Medicine, UNSW Medicine and Health, St Vincent’s Healthcare clinical campus, UNSW – sequence: 5 givenname: Stelios surname: Pavlidis fullname: Pavlidis, Stelios organization: The Airways Disease Section, National Heart & Lung Institute, Imperial College London – sequence: 6 givenname: Christina surname: Nalkurthi fullname: Nalkurthi, Christina organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney – sequence: 7 givenname: Prema M. surname: Nair fullname: Nair, Prema M. organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 8 givenname: Henry M. surname: Gomez fullname: Gomez, Henry M. organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 9 givenname: Irwan surname: Hanish fullname: Hanish, Irwan organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle, Department of Microbiology, Faculty of Biotechnology and Biomolecular Sciences, Universiti Putra Malaysia – sequence: 10 givenname: Alan CY surname: Hsu fullname: Hsu, Alan CY organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 11 givenname: Elinor surname: Hortle fullname: Hortle, Elinor organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney – sequence: 12 givenname: Sophie surname: Pickles fullname: Pickles, Sophie organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney – sequence: 13 givenname: Joselyn surname: Rojas-Quintero fullname: Rojas-Quintero, Joselyn organization: Department of Medicine, Baylor College of Medicine – sequence: 14 givenname: Raul San Jose surname: Estepar fullname: Estepar, Raul San Jose organization: Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School – sequence: 15 givenname: Jacqueline E. surname: Marshall fullname: Marshall, Jacqueline E. organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney – sequence: 16 givenname: Richard Y. surname: Kim fullname: Kim, Richard Y. organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle, School of Life Sciences, Faculty of Science, University of Technology Sydney – sequence: 17 givenname: Adam M. orcidid: 0000-0002-3074-3046 surname: Collison fullname: Collison, Adam M. organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 18 givenname: Joerg surname: Mattes fullname: Mattes, Joerg organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 19 givenname: Sobia surname: Idrees fullname: Idrees, Sobia organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney – sequence: 20 givenname: Alen orcidid: 0000-0003-1740-3538 surname: Faiz fullname: Faiz, Alen organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney – sequence: 21 givenname: Nicole G. surname: Hansbro fullname: Hansbro, Nicole G. organization: Centre for Inflammation, Centenary Institute, and Faculty of Science, University of Technology Sydney – sequence: 22 givenname: Ryutaro surname: Fukui fullname: Fukui, Ryutaro organization: Division of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo – sequence: 23 givenname: Yusuke orcidid: 0000-0001-6820-709X surname: Murakami fullname: Murakami, Yusuke organization: Faculty of Pharmacy, Department of Pharmaceutical Sciences, Musashino University – sequence: 24 givenname: Hong Sheng orcidid: 0000-0001-9745-7872 surname: Cheng fullname: Cheng, Hong Sheng organization: Lee Kong Chian School of Medicine, Nanyang Technological University – sequence: 25 givenname: Nguan Soon orcidid: 0000-0003-0136-7341 surname: Tan fullname: Tan, Nguan Soon organization: Lee Kong Chian School of Medicine, Nanyang Technological University, School of Biological Sciences, Nanyang Technological University – sequence: 26 givenname: Sanjay H. orcidid: 0000-0003-0417-7607 surname: Chotirmall fullname: Chotirmall, Sanjay H. organization: Lee Kong Chian School of Medicine, Nanyang Technological University, Department of Respiratory and Critical Care Medicine, Tan Tock Seng Hospital – sequence: 27 givenname: Jay C. surname: Horvat fullname: Horvat, Jay C. organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 28 givenname: Paul S. surname: Foster fullname: Foster, Paul S. organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 29 givenname: Brian GG surname: Oliver fullname: Oliver, Brian GG organization: Woolcock Institute of Medical Research, University of Sydney & School of Life Sciences, University of Technology – sequence: 30 givenname: Francesca surname: Polverino fullname: Polverino, Francesca organization: Department of Medicine, Baylor College of Medicine – sequence: 31 givenname: Antonio surname: Ieni fullname: Ieni, Antonio organization: Department of Human Pathology in Adult and Developmental Age “Gaetano Barresi”, Section of Anatomic Pathology, Università di Messina – sequence: 32 givenname: Francesco surname: Monaco fullname: Monaco, Francesco organization: Thoracic Surgery, Dipartimento di Scienze Biomediche, Odontoiatriche e delle Immagini Morfologiche e Funzionali (BIOMORF), Università di Messina – sequence: 33 givenname: Gaetano orcidid: 0000-0002-9807-327X surname: Caramori fullname: Caramori, Gaetano organization: Pneumologia, Dipartimento BIOMORF and Dipartimento di Medicina e Chirurgia, Universities of Messina and Parma – sequence: 34 givenname: Sukhwinder S. surname: Sohal fullname: Sohal, Sukhwinder S. organization: Respiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, University of Tasmania – sequence: 35 givenname: Ken R. orcidid: 0000-0001-5906-4605 surname: Bracke fullname: Bracke, Ken R. organization: Laboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital – sequence: 36 givenname: Peter A. surname: Wark fullname: Wark, Peter A. organization: Immune Healthy &/or Grow Up Well, Hunter Medical Research Institute & University of Newcastle – sequence: 37 givenname: Ian M. orcidid: 0000-0003-2101-8843 surname: Adcock fullname: Adcock, Ian M. organization: School of Clinical Medicine, UNSW Medicine and Health, St Vincent’s Healthcare clinical campus, UNSW – sequence: 38 givenname: Kensuke surname: Miyake fullname: Miyake, Kensuke organization: Division of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo – 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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37963864$$D View this record in MEDLINE/PubMed |
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| Snippet | Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke... Abstract Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke... |
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| Title | TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase |
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