The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD
| Autor: | Guy Brusselle, H. P. Van Eeckhoutte, E G De Smet, K Venken, Sharen Provoost, Pieter Mestdagh, Fien M. Verhamme, Stijn E. Verleden, Guy Joos, Tania Maes, F Avila Cobos, Ken R. Bracke, Evy E. Blomme |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
Lipopolysaccharide Immunology Inflammation Cigarette Smoking miR-155 Pathogenesis Mice Pulmonary Disease Chronic Obstructive chemistry.chemical_compound Immune system Macrophages Alveolar medicine Animals Humans Immunology and Allergy Mice Knockout COPD Lung business.industry Gene Expression Profiling Respiratory disease Pneumonia medicine.disease respiratory tract diseases Disease Models Animal MicroRNAs medicine.anatomical_structure Gene Expression Regulation Pulmonary Emphysema chemistry Cytokines Female RNA Interference Disease Susceptibility Human medicine Inflammation Mediators medicine.symptom business |
| Zdroj: | Mucosal immunology Europe PubMed Central |
| ISSN: | 1933-0219 |
| Popis: | Chronic obstructive pulmonary disease (COPD) is a highly prevalent respiratory disease characterized by airflow limitation and chronic inflammation. MiR-155 is described as an ancient regulator of the immune system. Our objective was to establish a role for miR-155 in cigarette smoke (CS)-induced inflammation and COPD. We demonstrate increased miR-155 expression by RT-qPCR in lung tissue of smokers without airflow limitation and patients with COPD compared to never smokers and in lung tissue and alveolar macrophages of CS-exposed mice compared to air-exposed mice. In addition, we exposed wild type and miR-155 deficient mice to CS and show an attenuated inflammatory profile in the latter. Alveolar macrophages were sorted by FACS from the different experimental groups and their gene expression profile was analyzed by RNA sequencing. This analysis revealed increased expression of miR-155 targets and an attenuation of the CS-induced increase in inflammation-related genes in miR-155 deficient mice. Moreover, intranasal instillation of a specific miR-155 inhibitor attenuated the CS-induced pulmonary inflammation in mice. Finally, elastase-induced emphysema and lung functional changes were significantly attenuated in miR-155 deficient mice. In conclusion, we highlight a role for miR-155 in CS-induced inflammation and the pathogenesis of COPD, implicating miR-155 as a new therapeutic target in COPD. |
| Databáze: | OpenAIRE |
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