Cigarette smoke and non-neuronal cholinergic system in the airway epithelium of COPD patients

Angela Marina Montalbano, Caterina Di Sano, Giuseppina Chiappara, Loredana Riccobono, Anna Bonanno, Giulia Anzalone, Patrizio Vitulo, Loredana Pipitone, Mark Gjomarkaj, Michael P Pieper, Fabio Luigi Massimo Ricciardolo, Rosalia Paola Gagliardo, Mirella Profita

Research output: Contribution to journalArticle

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Abstract

Acetylcholine (ACh), synthesized by Choline Acetyl-Transferase (ChAT), exerts its physiological effects via mAChRM3 in epithelial cells. We hypothesized that cigarette smoke affects ChAT, ACh, and mAChRM3 expression in the airways from COPD patients promoting airway disease. ChAT, ACh, and mAChRM3 were assessed: "ex vivo" in the epithelium from central and distal airways of COPD patients, Healthy Smoker (S) and Healthy Subjects (C), and "in vitro" in bronchial epithelial cells stimulated with cigarette smoke extract (CSE). In central airways, mAChRM3, ChAT, and ACh immunoreactivity was significantly higher in the epithelium from S and COPD than in C subjects. mAChRM3, ChAT, and ACh score of immunoreactivity was high in the metaplastia area of COPD patients. mAChRM3/ChAT and ACh/ChAT co-localization of immunoreactivity was observed in the bronchial epithelium from COPD. In vitro, CSE stimulation significantly increased mAChRM3, ChAT, and ACh expression and mAChRM3/ChAT and ACh/ChAT co-localization in 16HBE and NHBE, and increased 16HBE proliferation. Cigarette smoke modifies the levels of mAChMR3, ChAT expression, and ACh production in bronchial epithelial cells from COPD patients. Non-neuronal components of cholinergic system may have a role in the mechanism of bronchial epithelial cell proliferation, promoting alteration of normal tissue and of related pulmonary functions. This article is protected by copyright. All rights reserved.

Original languageEnglish
JournalJournal of Cellular Physiology
DOIs
Publication statusAccepted/In press - Nov 27 2017

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Transferases
Choline
Smoke
Tobacco Products
Chronic Obstructive Pulmonary Disease
Epithelium
Acetylcholine
Epithelial Cells
Non-Neuronal Cholinergic System
Healthy Volunteers
Cell Proliferation
Lung

Keywords

  • Journal Article

Cite this

Montalbano, A. M., Di Sano, C., Chiappara, G., Riccobono, L., Bonanno, A., Anzalone, G., ... Profita, M. (Accepted/In press). Cigarette smoke and non-neuronal cholinergic system in the airway epithelium of COPD patients. Journal of Cellular Physiology. https://doi.org/10.1002/jcp.26377

Cigarette smoke and non-neuronal cholinergic system in the airway epithelium of COPD patients. / Montalbano, Angela Marina; Di Sano, Caterina; Chiappara, Giuseppina; Riccobono, Loredana; Bonanno, Anna; Anzalone, Giulia; Vitulo, Patrizio; Pipitone, Loredana; Gjomarkaj, Mark; Pieper, Michael P; Ricciardolo, Fabio Luigi Massimo; Gagliardo, Rosalia Paola; Profita, Mirella.

In: Journal of Cellular Physiology, 27.11.2017.

Research output: Contribution to journalArticle

Montalbano, AM, Di Sano, C, Chiappara, G, Riccobono, L, Bonanno, A, Anzalone, G, Vitulo, P, Pipitone, L, Gjomarkaj, M, Pieper, MP, Ricciardolo, FLM, Gagliardo, RP & Profita, M 2017, 'Cigarette smoke and non-neuronal cholinergic system in the airway epithelium of COPD patients', Journal of Cellular Physiology. https://doi.org/10.1002/jcp.26377
Montalbano, Angela Marina ; Di Sano, Caterina ; Chiappara, Giuseppina ; Riccobono, Loredana ; Bonanno, Anna ; Anzalone, Giulia ; Vitulo, Patrizio ; Pipitone, Loredana ; Gjomarkaj, Mark ; Pieper, Michael P ; Ricciardolo, Fabio Luigi Massimo ; Gagliardo, Rosalia Paola ; Profita, Mirella. / Cigarette smoke and non-neuronal cholinergic system in the airway epithelium of COPD patients. In: Journal of Cellular Physiology. 2017.
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AU - Montalbano, Angela Marina

AU - Di Sano, Caterina

AU - Chiappara, Giuseppina

AU - Riccobono, Loredana

AU - Bonanno, Anna

AU - Anzalone, Giulia

AU - Vitulo, Patrizio

AU - Pipitone, Loredana

AU - Gjomarkaj, Mark

AU - Pieper, Michael P

AU - Ricciardolo, Fabio Luigi Massimo

AU - Gagliardo, Rosalia Paola

AU - Profita, Mirella

N1 - This article is protected by copyright. All rights reserved.

PY - 2017/11/27

Y1 - 2017/11/27

N2 - Acetylcholine (ACh), synthesized by Choline Acetyl-Transferase (ChAT), exerts its physiological effects via mAChRM3 in epithelial cells. We hypothesized that cigarette smoke affects ChAT, ACh, and mAChRM3 expression in the airways from COPD patients promoting airway disease. ChAT, ACh, and mAChRM3 were assessed: "ex vivo" in the epithelium from central and distal airways of COPD patients, Healthy Smoker (S) and Healthy Subjects (C), and "in vitro" in bronchial epithelial cells stimulated with cigarette smoke extract (CSE). In central airways, mAChRM3, ChAT, and ACh immunoreactivity was significantly higher in the epithelium from S and COPD than in C subjects. mAChRM3, ChAT, and ACh score of immunoreactivity was high in the metaplastia area of COPD patients. mAChRM3/ChAT and ACh/ChAT co-localization of immunoreactivity was observed in the bronchial epithelium from COPD. In vitro, CSE stimulation significantly increased mAChRM3, ChAT, and ACh expression and mAChRM3/ChAT and ACh/ChAT co-localization in 16HBE and NHBE, and increased 16HBE proliferation. Cigarette smoke modifies the levels of mAChMR3, ChAT expression, and ACh production in bronchial epithelial cells from COPD patients. Non-neuronal components of cholinergic system may have a role in the mechanism of bronchial epithelial cell proliferation, promoting alteration of normal tissue and of related pulmonary functions. This article is protected by copyright. All rights reserved.

AB - Acetylcholine (ACh), synthesized by Choline Acetyl-Transferase (ChAT), exerts its physiological effects via mAChRM3 in epithelial cells. We hypothesized that cigarette smoke affects ChAT, ACh, and mAChRM3 expression in the airways from COPD patients promoting airway disease. ChAT, ACh, and mAChRM3 were assessed: "ex vivo" in the epithelium from central and distal airways of COPD patients, Healthy Smoker (S) and Healthy Subjects (C), and "in vitro" in bronchial epithelial cells stimulated with cigarette smoke extract (CSE). In central airways, mAChRM3, ChAT, and ACh immunoreactivity was significantly higher in the epithelium from S and COPD than in C subjects. mAChRM3, ChAT, and ACh score of immunoreactivity was high in the metaplastia area of COPD patients. mAChRM3/ChAT and ACh/ChAT co-localization of immunoreactivity was observed in the bronchial epithelium from COPD. In vitro, CSE stimulation significantly increased mAChRM3, ChAT, and ACh expression and mAChRM3/ChAT and ACh/ChAT co-localization in 16HBE and NHBE, and increased 16HBE proliferation. Cigarette smoke modifies the levels of mAChMR3, ChAT expression, and ACh production in bronchial epithelial cells from COPD patients. Non-neuronal components of cholinergic system may have a role in the mechanism of bronchial epithelial cell proliferation, promoting alteration of normal tissue and of related pulmonary functions. This article is protected by copyright. All rights reserved.

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