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Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium

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Title: Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium
Authors: Vallese, D
Ricciardolo, FLM
Gnemmi, I
Casolari, P
Brun, P
Sorbello, V
Capelli, A
Cappello, F
Cavallesco, GN
Papi, A
Chung, KF
Balbi, B
Adcock, IM
Caramori, G
Di Stefano, A
Item Type: Journal Article
Abstract: Background: The role of mitogen-activated protein kinases (MAPK) in regulating the inflammatory response in the airways of patients with chronic obstructive pulmonary disease (COPD) and asthmatic patients is unclear. Objectives: To investigate the expression of activated MAPK in lungs of COPD patients and in bronchial biopsies of asthmatic patients and to study MAPK expression in bronchial epithelial cells in response to oxidative and inflammatory stimuli. Methods: Immunohistochemical expression of phospho (p)-p38 MAPK, p-JNK1 and p-ERK1/2 was measured in bronchial mucosa in patients with mild/moderate (n = 17), severe/very severe (n = 16) stable COPD, control smokers (n = 16), control non-smokers (n = 9), in mild asthma (n = 9) and in peripheral airways from COPD patients (n = 15) and control smokers (n = 15). Interleukin (IL)-8 and MAPK mRNA was measured in stimulated 16HBE cells. Results: No significant differences in p-p38 MAPK, p-JNK or p-ERK1/2 expression were seen in bronchial biopsies and peripheral airways between COPD and control subjects. Asthmatics showed increased submucosal p-p38 MAPK expression compared to COPD patients (p < 0.003) and control non-smokers (p < 0.05). Hydrogen peroxide (H2O2), cytomix (tumour necrosis factor-α + IL-1β + interferon-γ) and lipopolysaccharide (LPS) upregulated IL-8 mRNA at 1 or 2 h. p38 MAPKα mRNA was significantly increased after H2O2 and LPS treatment. JNK1 and ERK1 mRNA were unchanged after H2O2, cytomix or LPS treatments. Conclusion: p-p38 MAPK expression is similar in stable COPD and control subjects but increased in the bronchi of mild asthmatics compared to stable COPD patients. p38 MAPK mRNA is increased after bronchial epithelial challenges in vitro. These data together suggest a potential role for this MAPK in Th2 inflammation and possibly during COPD exacerbations.
Issue Date: 14-Mar-2015
Date of Acceptance: 2-Jan-2015
URI: http://hdl.handle.net/10044/1/51399
DOI: 10.1159/000375168
ISSN: 1423-0356
Publisher: Karger Publishers
Start Page: 329
End Page: 342
Journal / Book Title: Respiration
Volume: 89
Issue: 4
Keywords: Science & Technology
Life Sciences & Biomedicine
Respiratory System
Mitogen-activated protein kinases
p65
Pathology of chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease phenotypes
Asthma phenotypes
OBSTRUCTIVE PULMONARY-DISEASE
ACTIVATED PROTEIN-KINASE
P38 MAPK
OXIDATIVE STRESS
CELLS
PATHWAYS
SMOKE
MACROPHAGES
INHIBITION
SEVERITY
Aged
Asthma
Blotting, Western
Bronchi
Case-Control Studies
Cell Line
Female
Humans
Immunohistochemistry
Interleukin-8
Lymphocyte Count
Male
Middle Aged
Pulmonary Disease, Chronic Obstructive
Respiratory Mucosa
Transcription Factor RelA
p38 Mitogen-Activated Protein Kinases
Bronchi
Respiratory Mucosa
Cell Line
Humans
Asthma
Pulmonary Disease, Chronic Obstructive
p38 Mitogen-Activated Protein Kinases
Interleukin-8
Lymphocyte Count
Blotting, Western
Immunohistochemistry
Case-Control Studies
Aged
Middle Aged
Female
Male
Transcription Factor RelA
Science & Technology
Life Sciences & Biomedicine
Respiratory System
Mitogen-activated protein kinases
p65
Pathology of chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease phenotypes
Asthma phenotypes
OBSTRUCTIVE PULMONARY-DISEASE
ACTIVATED PROTEIN-KINASE
P38 MAPK
OXIDATIVE STRESS
CELLS
PATHWAYS
SMOKE
MACROPHAGES
INHIBITION
SEVERITY
1102 Cardiovascular Medicine And Haematology
Respiratory System
Publication Status: Published
Appears in Collections:National Heart and Lung Institute
Airway Disease
Faculty of Medicine



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