N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells

Abstract: Chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF) are lethal pulmonary diseases. Cigarette consumption is the main cause for development of COPD, while CF is produced by mutations in the CFTR gene. Although these diseases have a different etiology, both share a CFTR act...

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Autores principales: Valdivieso, Ángel Gabriel, Dugour, Andrea V., Sotomayor, Verónica, Clauzure, Mariángeles, Figueroa, Juan M., Santa Coloma, Tomás Antonio
Formato: Artículo
Lenguaje:Inglés
Publicado: Elsevier 2019
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Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/8661
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id I33-R139123456789-8661
record_format dspace
institution Universidad Católica Argentina
institution_str I-33
repository_str R-139
collection Repositorio Institucional de la Universidad Católica Argentina (UCA)
language Inglés
topic FIBROSIS QUISTICA
EPOC
ANTIOXIDANTES
spellingShingle FIBROSIS QUISTICA
EPOC
ANTIOXIDANTES
Valdivieso, Ángel Gabriel
Dugour, Andrea V.
Sotomayor, Verónica
Clauzure, Mariángeles
Figueroa, Juan M.
Santa Coloma, Tomás Antonio
N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells
topic_facet FIBROSIS QUISTICA
EPOC
ANTIOXIDANTES
description Abstract: Chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF) are lethal pulmonary diseases. Cigarette consumption is the main cause for development of COPD, while CF is produced by mutations in the CFTR gene. Although these diseases have a different etiology, both share a CFTR activity impairment and proinflammatory state even under sterile conditions. The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells. CSE treatment (100 µg/ml during 24 h) decreased CFTR mRNA expression and activity, and increased the release of IL-6 and IL-8. The effect on these cytokines was inhibited by N-acetyl cysteine (NAC, 5 mM) or the NF-kB inhibitor, IKK-2 (10 µM). CSE treatment also increased cellular and mitochondrial ROS levels. The cellular ROS levels were normalized to control values by NAC treatment, although significant effects on mitochondrial ROS levels were observed only at short times (5´) and effects on CFTR levels were not observed. In addition, CSE reduced the mitochondrial NADH-cytochrome c oxidoreductase (mCx I-III) activity, an effect that was not reverted by NAC. The reduced CFTR expression and the mitochondrial damage induced by CSE could not be normalized by NAC treatment, evidencing the need for a more specific reagent. In conclusion, CSE causes a sterile proinflammatory state and mitochondrial damage in Calu-3 cells that was partially recovered by NAC treatment.
format Artículo
author Valdivieso, Ángel Gabriel
Dugour, Andrea V.
Sotomayor, Verónica
Clauzure, Mariángeles
Figueroa, Juan M.
Santa Coloma, Tomás Antonio
author_facet Valdivieso, Ángel Gabriel
Dugour, Andrea V.
Sotomayor, Verónica
Clauzure, Mariángeles
Figueroa, Juan M.
Santa Coloma, Tomás Antonio
author_sort Valdivieso, Ángel Gabriel
title N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells
title_short N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells
title_full N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells
title_fullStr N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells
title_full_unstemmed N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells
title_sort n-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung calu-3 cells
publisher Elsevier
publishDate 2019
url https://repositorio.uca.edu.ar/handle/123456789/8661
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