MAP3K19 Is Overexpressed in COPD and Is a Central Mediator of Cigarette Smoke-Induced Pulmonary Inflammation and Lower Airway Destruction.
Identifieur interne : 000B73 ( Main/Exploration ); précédent : 000B72; suivant : 000B74MAP3K19 Is Overexpressed in COPD and Is a Central Mediator of Cigarette Smoke-Induced Pulmonary Inflammation and Lower Airway Destruction.
Auteurs : Stefen A. Boehme [États-Unis] ; Karin Franz-Bacon [États-Unis] ; John Ludka [États-Unis] ; Danielle N. Ditirro [États-Unis] ; Tai Wei Ly [États-Unis] ; Kevin B. Bacon [États-Unis]Source :
- PloS one [ 1932-6203 ] ; 2016.
Descripteurs français
- KwdFr :
- Adulte, Adulte d'âge moyen, Animaux, Appareil respiratoire (anatomopathologie), Appareil respiratoire (enzymologie), Appareil respiratoire (métabolisme), Broncho-pneumopathie chronique obstructive (enzymologie), Broncho-pneumopathie chronique obstructive (génétique), Broncho-pneumopathie chronique obstructive (métabolisme), Cellules HEK293, Cellules épithéliales (enzymologie), Cellules épithéliales (métabolisme), Cytokines (métabolisme), Expression des gènes, Facteur de transcription NF-kappa B (métabolisme), Femelle, Humains, Interférence par ARN, Lignée cellulaire tumorale, MAP Kinase Kinase Kinases (génétique), MAP Kinase Kinase Kinases (métabolisme), Macrophages (enzymologie), Mâle, Médiateurs de l'inflammation (métabolisme), Pneumopathie infectieuse (enzymologie), Pneumopathie infectieuse (génétique), Pneumopathie infectieuse (étiologie), RT-PCR, Souris, Souris de lignée BALB C, Sujet âgé, Sujet âgé de 80 ans ou plus, Tabagisme (effets indésirables), Technique de Western.
- MESH :
- anatomopathologie : Appareil respiratoire.
- effets indésirables : Tabagisme.
- enzymologie : Appareil respiratoire, Broncho-pneumopathie chronique obstructive, Cellules épithéliales, Macrophages, Pneumopathie infectieuse.
- génétique : Broncho-pneumopathie chronique obstructive, MAP Kinase Kinase Kinases, Pneumopathie infectieuse.
- métabolisme : Appareil respiratoire, Broncho-pneumopathie chronique obstructive, Cellules épithéliales, Cytokines, Facteur de transcription NF-kappa B, MAP Kinase Kinase Kinases, Médiateurs de l'inflammation.
- étiologie : Pneumopathie infectieuse.
- Adulte, Adulte d'âge moyen, Animaux, Cellules HEK293, Expression des gènes, Femelle, Humains, Interférence par ARN, Lignée cellulaire tumorale, Mâle, RT-PCR, Souris, Souris de lignée BALB C, Sujet âgé, Sujet âgé de 80 ans ou plus, Technique de Western.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Animals, Blotting, Western, Cell Line, Tumor, Cytokines (metabolism), Epithelial Cells (enzymology), Epithelial Cells (metabolism), Female, Gene Expression, HEK293 Cells, Humans, Inflammation Mediators (metabolism), MAP Kinase Kinase Kinases (genetics), MAP Kinase Kinase Kinases (metabolism), Macrophages (enzymology), Male, Mice, Mice, Inbred BALB C, Middle Aged, NF-kappa B (metabolism), Pneumonia (enzymology), Pneumonia (etiology), Pneumonia (genetics), Pulmonary Disease, Chronic Obstructive (enzymology), Pulmonary Disease, Chronic Obstructive (genetics), Pulmonary Disease, Chronic Obstructive (metabolism), RNA Interference, Respiratory System (enzymology), Respiratory System (metabolism), Respiratory System (pathology), Reverse Transcriptase Polymerase Chain Reaction, Smoking (adverse effects).
- MESH :
- chemical , genetics : MAP Kinase Kinase Kinases.
- chemical , metabolism : Cytokines, Inflammation Mediators, MAP Kinase Kinase Kinases, NF-kappa B.
- adverse effects : Smoking.
- enzymology : Epithelial Cells, Macrophages, Pneumonia, Pulmonary Disease, Chronic Obstructive, Respiratory System.
- etiology : Pneumonia.
- genetics : Pneumonia, Pulmonary Disease, Chronic Obstructive.
- metabolism : Epithelial Cells, Pulmonary Disease, Chronic Obstructive, Respiratory System.
- pathology : Respiratory System.
- Adult, Aged, Aged, 80 and over, Animals, Blotting, Western, Cell Line, Tumor, Female, Gene Expression, HEK293 Cells, Humans, Male, Mice, Mice, Inbred BALB C, Middle Aged, RNA Interference, Reverse Transcriptase Polymerase Chain Reaction.
Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation and lung inflammation resulting in a progressive decline in lung function whose principle cause is cigarette smoke. MAP3K19 is a novel kinase expressed predominantly by alveolar and interstitial macrophages and bronchial epithelial cells in the lung. We found that MAP3K19 mRNA was overexpressed in a limited sampling of lung tissue from COPD patients, and a closer examination found it to be overexpressed in bronchoalveolar macrophages from COPD patients, as well as the bronchial epithelium and inflammatory cells in the lamina propria. We further found MAP3K19 to be induced in various cell lines upon environmental stress, such as cigarette smoke, oxidative and osmotic stress. Exogenous expression of MAP3K19 in cells caused an upregulation of transcriptionally active NF-κB, and secretion of the chemokines CXCL-8, CCL-20 and CCL-7. Inhibition of MAP3K19 activity by siRNA or small molecular weight inhibitors caused a decrease in cigarette smoke-induced inflammation in various murine models, which included a decrease in pulmonary neutrophilia and KC levels. In a chronic cigarette smoke model, inhibition of MAP3K19 significantly attenuated emphysematous changes in airway parenchyma. Finally, in a viral exacerbation model, mice exposed to cigarette smoke and influenza A virus showed a decrease in pulmonary neutrophilia, pro-inflammatory cytokines and viral load upon inhibition of MAP3K19. Collectively, these results suggest that inhibition of MAP3K19 may represent a novel strategy to target COPD that promises to have a potential therapeutic benefit for patients.
DOI: 10.1371/journal.pone.0167169
PubMed: 27935962
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation and lung inflammation resulting in a progressive decline in lung function whose principle cause is cigarette smoke. MAP3K19 is a novel kinase expressed predominantly by alveolar and interstitial macrophages and bronchial epithelial cells in the lung. We found that MAP3K19 mRNA was overexpressed in a limited sampling of lung tissue from COPD patients, and a closer examination found it to be overexpressed in bronchoalveolar macrophages from COPD patients, as well as the bronchial epithelium and inflammatory cells in the lamina propria. We further found MAP3K19 to be induced in various cell lines upon environmental stress, such as cigarette smoke, oxidative and osmotic stress. Exogenous expression of MAP3K19 in cells caused an upregulation of transcriptionally active NF-κB, and secretion of the chemokines CXCL-8, CCL-20 and CCL-7. Inhibition of MAP3K19 activity by siRNA or small molecular weight inhibitors caused a decrease in cigarette smoke-induced inflammation in various murine models, which included a decrease in pulmonary neutrophilia and KC levels. In a chronic cigarette smoke model, inhibition of MAP3K19 significantly attenuated emphysematous changes in airway parenchyma. Finally, in a viral exacerbation model, mice exposed to cigarette smoke and influenza A virus showed a decrease in pulmonary neutrophilia, pro-inflammatory cytokines and viral load upon inhibition of MAP3K19. Collectively, these results suggest that inhibition of MAP3K19 may represent a novel strategy to target COPD that promises to have a potential therapeutic benefit for patients.</div>
</front>
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