Nicotine promotes chronic obstructive pulmonary disease via inducing pyroptosis activation in bronchial epithelial cells

Mo, Rubing; Zhang, Jun; Chen, Yongxing; Ding, Yipeng

doi:10.3892/mmr.2022.12608

Cited by 19 publications

(9 citation statements)

References 52 publications

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“…The persistent airway inflammation causes airway remodeling, which is characterized by sloughing of BECs, mucus hypersecretion, and abnormal deposition of collagen [ 37 ]. A large body of evidence suggests that cigarette smoke (CS) is the predominant risk factor for COPD [ 47 , 89 ].…”

Section: Pyroptosis and Inflammation-related Respiratory Diseasesmentioning

confidence: 99%

“…Currently, it is shown that CS extract (CSE) activates the NLRP3/caspase-1/GSDMD signaling pathway and sequentially induces pyroptosis in BECs, which causes the impaired BEC barrier and severe lung injury [ 74 ]. Inhibiting the NLRP3 inflammasome results in the downregulation of GSDMD, which causes pyroptosis, as well as the alleviation of pulmonary inflammation [ 47 , 89 ]. Furthermore, accumulating studies suggest that pyroptosis is activated by CS-induced ERS via ROS and participates in the progression of COPD [ 41 , 89 ].…”

Section: Pyroptosis and Inflammation-related Respiratory Diseasesmentioning

confidence: 99%

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Pyroptosis in inflammation-related respiratory disease

Feng

Yangzhong

et al. 2022

J Physiol Biochem

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Pyroptosis is commonly induced by the gasdermin (GSDM) family and is accompanied by the release of inflammatory cytokines such as IL-1β and IL-18. Recently, increasing evidence suggests that pyroptosis plays a role in respiratory diseases. This review aimed to summarize the roles and mechanisms of pyroptosis in inflammation-related respiratory diseases. There are several pathways involved in pyroptosis, such as the canonical inflammasome-induced pathway, non-canonical inflammasome-induced pathway, caspase-1/3/6/7/GSDMB pathway, caspase-8/GSDMC pathway, caspase-8/GSDMD pathway, and caspase-3/GSEME pathway. Pyroptosis may be involved in asthma, chronic obstructive pulmonary disease (COPD), lung cancer, acute lung injury (ALI), silicosis, pulmonary hypertension (PH), and tuberculosis (TB), in which the NLRP3 inflammasome-induced pathway is mostly highlighted. Pyroptosis contributes to the deterioration of asthma, COPD, ALI, silicosis, and PH. In addition, pyroptosis has dual effects on lung cancer and TB. Additionally, whether pyroptosis participates in cystic fibrosis (CF) and sarcoidosis or not is largely unknown, though the activation of NLRP3 inflammasome is found in CF and sarcoidosis. In conclusion, pyroptosis may play a role in inflammation-related respiratory diseases, providing new therapeutic targets.

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Section: Pyroptosis and Inflammation-related Respiratory Diseasesmentioning

confidence: 99%

Section: Pyroptosis and Inflammation-related Respiratory Diseasesmentioning

confidence: 99%

Pyroptosis in inflammation-related respiratory disease

Feng

Yangzhong

et al. 2022

J Physiol Biochem

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“…Pyroptosis is a type of programmed cell death mediated by the inflammatory caspases. The release of cell contents caused by pyroptosis will aggravate the inflammatory response to further deteriorate COPD [ 10 ]. Pyroptosis represents a unique cell death form usually activated by the NOD‑like receptor protein‑3 (NLRP3) inflammasome and Caspase‑1 [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Nrf2/HO-1 signaling activation alleviates cigarette smoke-induced inflammation in chronic obstructive pulmonary disease by suppressing NLRP3-mediated pyroptosis

Zhang,

Wang,

Wang

et al. 2024

J Cardiothorac Surg

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Background This study examined the effect of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway on chronic obstructive pulmonary disease (COPD) and the potential molecular mechanism. Methods A COPD mouse model was established by cigarette smoke exposure and administered with either ML385 or dimethyl fumarate (DMF). Airway resistance of mice was detected. IL-1β and IL-6 levels in mice alveolar lavage fluid were examined by enzyme-linked immunosorbent assay. Hematoxylin and eosin staining and immunohistochemical of lung tissues were utilized to detect lung injury and NLRP3 expression. DMF was used to treat COPD cell model constructed by exposing normal human bronchial epithelial (NHBE) cells to cigarette smoke extract. NHBE cells were transfected by NLRP3-expression vectors. Expression of proteins was detected by Western blot. Results COPD mice showed the enhanced airway resistance, the inactivated Nrf2/HO-1 pathway and the overexpressed NLRP3, Caspase-1 and GSDMD-N proteins in lung tissues, and the increased IL-1β and IL-6 levels in alveolar lavage fluid. ML385 treatment augmented these indicators and lung injury in COPD mice. However, DMF intervention attenuated these indicators and lung injury in COPD mice. Nrf2/HO-1 pathway inactivation and overexpression of NLRP3, Caspase-1 and GSDMD-N proteins were observed in COPD cells. DMF intervention activated Nrf2/HO-1 pathway and down-regulated NLRP3, Caspase-1 and GSDMD-N proteins in COPD cells. However, NLRP3 overexpression abolished the effect of DMF on COPD cells. Conclusion Nrf2/HO-1 pathway activation may alleviate inflammation in COPD by suppressing the NLRP3-related pyroptosis. Activating the Nrf2/HO-1 pathway may be an effective method to treat COPD.

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“…Cigarette smoking can relieve stress and decrease subjective anxiety [ 1 – 5 ]. However, nicotine, the main chemical in cigarettes, affects lung function and leads to chronic obstructive pulmonary disease (COPD) [ 6 , 7 ]. Furthermore, smoking is also associated with diabetes because of its deleterious effects on pancreatic functions [ 8 – 10 ].…”

Section: Introductionmentioning

confidence: 99%

Epigenetic age acceleration mediates the association between smoking and diabetes-related outcomes

Chang

Lin

2023

Clin Epigenet

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Background Smoking can lead to the deterioration of lung function and susceptibility to diabetes. Recently, smoking was found to induce DNA methylation (DNAm) changes in some cytosine-phosphate-guanine sites (CpGs). As linear combinations of DNAm levels of aging-related CpGs, five measures of epigenetic age acceleration (EAA) have received extensive attention: HannumEAA, IEAA, PhenoEAA, GrimEAA, and DunedinPACE. It is of interest to explore whether some measures of EAA can mediate the associations of smoking with diabetes-related outcomes and indices of ventilatory lung function. Methods and results In this study, we included self-reported smoking variables (smoking status, the number of pack-years, and years since smoking cessation), seven DNAm markers (HannumEAA, IEAA, PhenoEAA, GrimEAA, DNAm-based smoking pack-years, DNAm plasminogen activator inhibitor 1 [PAI-1] levels, and DunedinPACE), and four health outcomes (fasting glucose, hemoglobin A1C, forced expiratory volume in 1.0 s [FEV1], and forced vital capacity [FVC]) from 2474 Taiwan Biobank participants. Mediation analyses were conducted while adjusting for chronological age, sex, body mass index, drinking status, regular exercise status, educational attainment, and five cell-type proportions. We demonstrated that GrimEAA, DNAm-based smoking pack-years, DNAm PAI-1 levels, DunedinPACE, and PhenoEAA mediated smoking associations with diabetes-related outcomes. Moreover, current and former smoking both had an adverse indirect effect on FVC through DNAm PAI-1 levels. For former smokers, a long time since smoking cessation had a positive indirect impact on FVC through GrimEAA and on FEV1 through PhenoEAA. Conclusions This is one of the first studies to comprehensively investigate the role of five measures of EAA in mediating the associations of smoking with the health outcomes of an Asian population. The results showed that the second-generation epigenetic clocks (GrimEAA, DunedinPACE, and PhenoEAA) significantly mediated the associations between smoking and diabetes-related outcomes. In contrast, the first-generation epigenetic clocks (HannumEAA and IEAA) did not significantly mediate any associations of smoking variables with the four health outcomes. Cigarette smoking can, directly and indirectly, deteriorate human health through DNAm changes in aging-related CpG sites.

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Nicotine promotes chronic obstructive pulmonary disease via inducing pyroptosis activation in bronchial epithelial cells

Cited by 19 publications

References 52 publications

Pyroptosis in inflammation-related respiratory disease

Pyroptosis in inflammation-related respiratory disease

Nrf2/HO-1 signaling activation alleviates cigarette smoke-induced inflammation in chronic obstructive pulmonary disease by suppressing NLRP3-mediated pyroptosis

Epigenetic age acceleration mediates the association between smoking and diabetes-related outcomes

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