ArticleRedox biology2018
N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Effects of Intrauterine Isoproterenol Administration on Ovarian Follicular Development in Cows.Veterinary medicine and science · 2025Article
- BTG2-deficient mast cells remodel the tumor and tumor-draining lymph node microenvironment leading to chemotherapy resistance in breast cancer.Frontiers in immunology · 2025Article
- From CFTR to a CF signalling network: a systems biology approach to study Cystic Fibrosis.BMC genomics · 2024Article
- NLRP10 promotes AGEs-induced NLRP1 and NLRP3 inflammasome activation via ROS/MAPK/NF-κB signaling in human periodontal ligament cells.Odontology · 2024Article
- Article
- Vx-809, a CFTR Corrector, Acts through a General Mechanism of Protein Folding and on the Inflammatory Process.International journal of molecular sciences · 2023Article
- Review
- Article
- Treatment with Bixin-Loaded Polymeric Nanoparticles Prevents Cigarette Smoke-Induced Acute Lung Inflammation and Oxidative Stress in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Dysregulated mitochondrial metabolism upon cigarette smoke exposure in various human bronchial epithelial cell models.Disease models & mechanisms · 2022Article
- NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) modulation by intracellular ClImmunology · 2021Article
- Effects of N-acetyl cysteine on mitochondrial ROS, mitochondrial dynamics, and inflammation on lipopolysaccharide-treated human apical papilla cells.Clinical oral investigations · 2021Article
- Lumacaftor and Matrine: Possible Therapeutic Combination to Counteract the Inflammatory Process in Cystic Fibrosis.Biomolecules · 2021Article
- Retrograde signaling by a mtDNA-encoded non-coding RNA preserves mitochondrial bioenergetics.Communications biology · 2020Article
- Mitochondria: at the crossroads of regulating lung epithelial cell function in chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2020Review
- Modeling cellular metabolomic effects of oxidative stress impacts from hydrogen peroxide and cigarette smoke on human lung epithelial cells.Journal of breath research · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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