Type 2 inflammation in asthma and other airway diseases
Chronic inflammatory airway diseases, including asthma, chronic rhinosinusitis, eosinophilic COPD and allergic rhinitis are a global health concern. Despite the coexistence of these diseases and their common pathophysiology, they are often managed independently, resulting in poor asthma control, con...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Respiratory Society
2022-08-01
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| Series: | ERJ Open Research |
| Online Access: | http://openres.ersjournals.com/content/8/3/00576-2021.full |
| _version_ | 1797809466353123328 |
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| author | Jorge Maspero Yochai Adir Mona Al-Ahmad Carlos A. Celis-Preciado Federico D. Colodenco Pedro Giavina-Bianchi Hani Lababidi Olivier Ledanois Bassam Mahoub Diahn-Warng Perng Juan C. Vazquez Arzu Yorgancioglu |
| author_facet | Jorge Maspero Yochai Adir Mona Al-Ahmad Carlos A. Celis-Preciado Federico D. Colodenco Pedro Giavina-Bianchi Hani Lababidi Olivier Ledanois Bassam Mahoub Diahn-Warng Perng Juan C. Vazquez Arzu Yorgancioglu |
| author_sort | Jorge Maspero |
| collection | DOAJ |
| description | Chronic inflammatory airway diseases, including asthma, chronic rhinosinusitis, eosinophilic COPD and allergic rhinitis are a global health concern. Despite the coexistence of these diseases and their common pathophysiology, they are often managed independently, resulting in poor asthma control, continued symptoms and poor quality of life. Understanding disease pathophysiology is important for best treatment practice, reduced disease burden and improved patient outcomes. The pathophysiology of type 2 inflammation is driven by both the innate immune system triggered by pollutants, viral or fungal infections involving type 2 innate lymphoid cells (ILC2) and the adaptive immune system, triggered by contact with an allergen involving type 2 T-helper (Th2) cells. Both ILC2 and Th2 cells produce the type-2 cytokines (interleukin (IL)-4, IL-5 and IL-13), each with several roles in the inflammation cascade. IL-4 and IL-13 cause B-cell class switching and IgE production, release of pro-inflammatory mediators, barrier disruption and tissue remodelling. In addition, IL-13 causes goblet-cell hyperplasia and mucus production. All three interleukins are involved in trafficking eosinophils to tissues, producing clinical symptoms characteristic of chronic inflammatory airway diseases. Asthma is a heterogenous disease; therefore, identification of biomarkers and early targeted treatment is critical for patients inadequately managed by inhaled corticosteroids and long-acting β-agonists alone. The Global Initiative for Asthma guidelines recommend add-on biological (anti IgE, IL-5/5R, IL-4R) treatments for those not responding to standard of care. Targeted therapies, including omalizumab, mepolizumab, reslizumab, benralizumab, dupilumab and tezepelumab, were developed on current understanding of the pathophysiology of type 2 inflammation. These therapies offer hope for improved management of type 2 inflammatory airway diseases. |
| first_indexed | 2024-03-13T06:53:13Z |
| format | Article |
| id | doaj.art-e484d8b4f20241e3940b1f231c35449d |
| institution | Directory Open Access Journal |
| issn | 2312-0541 |
| language | English |
| last_indexed | 2024-03-13T06:53:13Z |
| publishDate | 2022-08-01 |
| publisher | European Respiratory Society |
| record_format | Article |
| series | ERJ Open Research |
| spelling | doaj.art-e484d8b4f20241e3940b1f231c35449d2023-06-07T13:30:19ZengEuropean Respiratory SocietyERJ Open Research2312-05412022-08-018310.1183/23120541.00576-202100576-2021Type 2 inflammation in asthma and other airway diseasesJorge Maspero0Yochai Adir1Mona Al-Ahmad2Carlos A. Celis-Preciado3Federico D. Colodenco4Pedro Giavina-Bianchi5Hani Lababidi6Olivier Ledanois7Bassam Mahoub8Diahn-Warng Perng9Juan C. Vazquez10Arzu Yorgancioglu11 Fundacion CIDEA (Centro de Investigacion de Enfermedades Alergicas y Respiratorias), University of Buenos Aires, Buenos Aires, Argentina Pulmonary Division, Lady Davis Carmel Medical Center, Faculty of Medicine, The Technion, Institute of Technology, Haifa, Israel Microbiology Dept, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait Pulmonary Unit, Internal Medicine Department, Hospital Universitario San Ignacio, Bogota, Colombia Pulmonology, Hospital De Rehabilitación Respiratoria María Ferrer, Buenos Aires, Argentina Clinical Immunology and Allergy Division, University of Sao Paulo, Sao Paulo, Brazil King Fahad Medical City, Riyadh, Saudi Arabia Sanofi Genzyme, Paris, France Dept of Pulmonary Medicine and Allergy and Sleep Medicine, Rashid Hospital, Dubai, United Arab Emirates Taipei Veterans General Hospital, Taipei, Taiwan Instituto Nacional de Enfermedades Respiratorias, Mexico City, Mexico Dept of Chest Diseases, Faculty of Medicine, Manisa Celal Bayar University, Manisa, Turkey Chronic inflammatory airway diseases, including asthma, chronic rhinosinusitis, eosinophilic COPD and allergic rhinitis are a global health concern. Despite the coexistence of these diseases and their common pathophysiology, they are often managed independently, resulting in poor asthma control, continued symptoms and poor quality of life. Understanding disease pathophysiology is important for best treatment practice, reduced disease burden and improved patient outcomes. The pathophysiology of type 2 inflammation is driven by both the innate immune system triggered by pollutants, viral or fungal infections involving type 2 innate lymphoid cells (ILC2) and the adaptive immune system, triggered by contact with an allergen involving type 2 T-helper (Th2) cells. Both ILC2 and Th2 cells produce the type-2 cytokines (interleukin (IL)-4, IL-5 and IL-13), each with several roles in the inflammation cascade. IL-4 and IL-13 cause B-cell class switching and IgE production, release of pro-inflammatory mediators, barrier disruption and tissue remodelling. In addition, IL-13 causes goblet-cell hyperplasia and mucus production. All three interleukins are involved in trafficking eosinophils to tissues, producing clinical symptoms characteristic of chronic inflammatory airway diseases. Asthma is a heterogenous disease; therefore, identification of biomarkers and early targeted treatment is critical for patients inadequately managed by inhaled corticosteroids and long-acting β-agonists alone. The Global Initiative for Asthma guidelines recommend add-on biological (anti IgE, IL-5/5R, IL-4R) treatments for those not responding to standard of care. Targeted therapies, including omalizumab, mepolizumab, reslizumab, benralizumab, dupilumab and tezepelumab, were developed on current understanding of the pathophysiology of type 2 inflammation. These therapies offer hope for improved management of type 2 inflammatory airway diseases.http://openres.ersjournals.com/content/8/3/00576-2021.full |
| spellingShingle | Jorge Maspero Yochai Adir Mona Al-Ahmad Carlos A. Celis-Preciado Federico D. Colodenco Pedro Giavina-Bianchi Hani Lababidi Olivier Ledanois Bassam Mahoub Diahn-Warng Perng Juan C. Vazquez Arzu Yorgancioglu Type 2 inflammation in asthma and other airway diseases ERJ Open Research |
| title | Type 2 inflammation in asthma and other airway diseases |
| title_full | Type 2 inflammation in asthma and other airway diseases |
| title_fullStr | Type 2 inflammation in asthma and other airway diseases |
| title_full_unstemmed | Type 2 inflammation in asthma and other airway diseases |
| title_short | Type 2 inflammation in asthma and other airway diseases |
| title_sort | type 2 inflammation in asthma and other airway diseases |
| url | http://openres.ersjournals.com/content/8/3/00576-2021.full |
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