Theaflavin‑3,3'‑digallate attenuates cigarette smoke extract‑induced pulmonary emphysema in mice by suppressing necroptosis

Luan, Guangxin; Zhu, Zhen; Wu, Kaiyue; Yin, Shi

doi:10.3892/etm.2021.10933

“…The classical mouse model of COPD makes use of lipopolysaccharide, PPE, elastase, and cigarette smoke extract (CSE) [ 23 ]. The intraperitoneal injection or inhalation of CSE can induce airway inflammation [ 24 , 25 ]. However, exposure to CSE and allergens does not yield consistent airway inflammation and airway resistance [ 21 , 26 – 28 ].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of asthma–chronic obstructive pulmonary disease overlap using a mouse model of pulmonary disease

Jo

¹

,

Rhee

²

,

Yoon

³

et al. 2022

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Background Features of asthma and chronic obstructive pulmonary disease (COPD) can coexist in the same patient, in a condition termed asthma– chronic obstructive pulmonary disease overlap (ACO). ACO is heterogeneous condition exhibiting various combinations of asthma and COPD features. No clinically acceptable experimental model of ACO has been established. We aimed to establish an animal model of ACO. Methods We generated two phenotypes of ACO by administering ovalbumin and porcine pancreatic elastase in combination, and papain. The proinflammatory cytokines and cell types in bronchoalveolar lavage fluid (BALF) were investigated, and lung function parameters were measured using the FlexiVent system. Results Greater airway inflammation was observed in the asthma and both ACO models, and emphysema was found in the COPD and both ACO models. The proportion of eosinophils in BALF was elevated in the asthma and ACO-a model. Type 2 inflammatory cytokine levels were highest in the ACO-a model, and the neutrophil gelatinase–associated lipocalin level was elevated in the asthma and ACO-a model. Of lung function parameters, compliance was greater in the COPD and ACO-b model, in which elastance was lower than in the asthma model. Airway resistance increased with the methacholine concentration in the asthma and both ACO models, but not in the control or COPD model. Conclusion We established two murine models of ACO that exhibit features of asthma and COPD. We validated the clinical relevance of the ACO models based on changes in cytokine profiles and lung function. These models will be useful in further studies of the pathogenesis of, and therapeutic targets for ACO.

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“…The pro-inflammatory cytokine IL-1 is catalysed by capase-1 from activated NLRP3 inflammasome. The protective effects of theaflavin-3,3'-digallate might inhibit NLRP3 pathways [79].…”

Section: Polyphenols Treatment Via Inflammasome In a Cigarette Smokin...mentioning

confidence: 99%

Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD

Fu¹,

Kang²,

Yan³

et al. 2022

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COPD is predicted to become the third leading cause of morbidity and mortality worldwide by 2030. Cigarette smoking (active or passive) is one of its chief causes, with about 20% of cigarette smokers developing COPD from cigarette smoke (CS)-induced irreversible damage and sustained inflammation of the airway epithelium. Inflammasome activation leads to the cleavage of pro-interleukin (IL)-1β and pro-IL-18, along with the release of pro-inflammatory cytokines via gasdermin D N-terminal fragment membrane pores, which further triggers acute phase pro-inflammatory responses and concurrent pyroptosis. There is currently intense interest in the role of nucleotide-binding oligomerisation domain-like receptor family, pyrin domain containing protein-3 inflammasomes in chronic inflammatory lung diseases such as COPD and their potential for therapeutic targeting. Phytochemicals including polyphenols and flavonoids have phyto-medicinal benefits in CS-COPD. Here, we review published articles from the last decade regarding the known associations between inflammasome-mediated responses and ameliorations in pre-clinical manifestations of CS-COPD via polyphenol and flavonoid treatment, with a focus on the underlying mechanistic insights. This article will potentially assist the development of drugs for the prevention and therapy of COPD, particularly in cigarette smokers.

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“…The classical mouse model of COPD makes use of lipopolysaccharide, PPE, elastase, and cigarette smoke extract (CSE) (23). The intraperitoneal injection or inhalation of CSE can induce airway in ammation (24,25). However, exposure to CSE and allergens does not yield consistent airway in ammation and airway resistance (21,(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of asthma–chronic obstructive pulmonary disease overlap using a mouse model of pulmonary disease

Jo

¹

,

Rhee

²

,

Yoon

³

et al. 2022

Preprint

0

View full text Add to dashboard Cite

Background Features of asthma and chronic obstructive pulmonary disease (COPD) can coexist in the same patient, in a condition termed asthma– chronic obstructive pulmonary disease overlap (ACO). ACO is heterogeneous condition exhibiting various combinations of asthma and COPD features. No clinically acceptable experimental model of ACO has been established. We aimed to establish an animal model of ACO. Methods We generated two phenotypes of ACO by administering ovalbumin and porcine pancreatic elastase in combination, and papain. The proinflammatory cytokines and cell types in bronchoalveolar lavage fluid (BALF) were investigated, and lung function parameters were measured using the FlexiVent system. Results Greater airway inflammation was observed in the asthma and both ACO models, and emphysema was found in the COPD and both ACO models. The proportion of eosinophils in BALF was elevated in the asthma and ACO-a model. Type 2 inflammatory cytokine levels were highest in the ACO-a model, and the neutrophil gelatinase–associated lipocalin level was elevated in the asthma and ACO-a model. Of lung function parameters, compliance was greater in the COPD and ACO-b model, in which elastance was lower than in the asthma model. Airway resistance increased with the methacholine concentration in the asthma and both ACO models, but not in the control or COPD model. Conclusion We established two murine models of ACO that exhibit features of asthma and COPD. We validated the clinical relevance of the ACO models based on changes in cytokine profiles and lung function. These models will be useful in further studies of the pathogenesis of, and therapeutic targets for ACO.

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Theaflavin‑3,3'‑digallate attenuates cigarette smoke extract‑induced pulmonary emphysema in mice by suppressing necroptosis

Cited by 10 publications

References 29 publications

Evaluation of asthma–chronic obstructive pulmonary disease overlap using a mouse model of pulmonary disease

Evaluation of asthma–chronic obstructive pulmonary disease overlap using a mouse model of pulmonary disease

Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD

Evaluation of asthma–chronic obstructive pulmonary disease overlap using a mouse model of pulmonary disease

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