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The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD

Elise De Smet, Hannelore Van Eeckhoutte (UGent) , Francisco Avila Cobos (UGent) , Evy Blomme (UGent) , Fien Verhamme (UGent) , Sharen Provoost (UGent) , Stijn Verleden (UGent) , Koen Venken (UGent) , Tania Maes (UGent) , Guy Joos (UGent) , et al.
(2020) MUCOSAL IMMUNOLOGY. 13(3). p.423-436
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Abstract
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.
Keywords
Immunology, Immunology and Allergy, NF-KAPPA-B, MICRORNA-155 PROMOTES, ALVEOLAR MACROPHAGES, EXPERIMENTAL COLITIS, CYTOKINE RELEASE, PATHOGENESIS, CELLS, LIPOPOLYSACCHARIDE, DIFFERENTIATION, INHIBITION

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MLA
De Smet, Elise, et al. “The Role of MiR-155 in Cigarette Smoke-Induced Pulmonary Inflammation and COPD.” MUCOSAL IMMUNOLOGY, vol. 13, no. 3, 2020, pp. 423–36.
APA
De Smet, E., Van Eeckhoutte, H., Avila Cobos, F., Blomme, E., Verhamme, F., Provoost, S., … Bracke, K. (2020). The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD. MUCOSAL IMMUNOLOGY, 13(3), 423–436.
Chicago author-date
De Smet, Elise, Hannelore Van Eeckhoutte, Francisco Avila Cobos, Evy Blomme, Fien Verhamme, Sharen Provoost, Stijn Verleden, et al. 2020. “The Role of MiR-155 in Cigarette Smoke-Induced Pulmonary Inflammation and COPD.” MUCOSAL IMMUNOLOGY 13 (3): 423–36.
Chicago author-date (all authors)
De Smet, Elise, Hannelore Van Eeckhoutte, Francisco Avila Cobos, Evy Blomme, Fien Verhamme, Sharen Provoost, Stijn Verleden, Koen Venken, Tania Maes, Guy Joos, Pieter Mestdagh, Guy Brusselle, and Ken Bracke. 2020. “The Role of MiR-155 in Cigarette Smoke-Induced Pulmonary Inflammation and COPD.” MUCOSAL IMMUNOLOGY 13 (3): 423–436.
Vancouver
1.
De Smet E, Van Eeckhoutte H, Avila Cobos F, Blomme E, Verhamme F, Provoost S, et al. The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD. MUCOSAL IMMUNOLOGY. 2020;13(3):423–36.
IEEE
[1]
E. De Smet et al., “The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD,” MUCOSAL IMMUNOLOGY, vol. 13, no. 3, pp. 423–436, 2020.
@article{8656828,
  abstract     = {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.},
  author       = {De Smet, Elise and Van Eeckhoutte, Hannelore and Avila Cobos, Francisco and Blomme, Evy and Verhamme, Fien and Provoost, Sharen and Verleden, Stijn and Venken, Koen and Maes, Tania and Joos, Guy and Mestdagh, Pieter and Brusselle, Guy and Bracke, Ken},
  issn         = {1933-0219},
  journal      = {MUCOSAL IMMUNOLOGY},
  keywords     = {Immunology,Immunology and Allergy,NF-KAPPA-B,MICRORNA-155 PROMOTES,ALVEOLAR MACROPHAGES,EXPERIMENTAL COLITIS,CYTOKINE RELEASE,PATHOGENESIS,CELLS,LIPOPOLYSACCHARIDE,DIFFERENTIATION,INHIBITION},
  language     = {eng},
  number       = {3},
  pages        = {423--436},
  title        = {The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD},
  url          = {http://dx.doi.org/10.1038/s41385-019-0241-6},
  volume       = {13},
  year         = {2020},
}

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