Neutrophil extracellular traps induced by cigarette smoke contribute to airway inflammation in mice

Zou, Yong; Chen, Xi; He, Ben; Xiao, Jian; Ye, Qiao; Xie, Baohua; Yang, Shasha; Dai, Longxia; Dai, Ziyu; Chen, Qiong

doi:10.1016/j.yexcr.2020.111888

Cited by 26 publications

(21 citation statements)

References 36 publications

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“…Bronchial epithelial cells are one of the key cell types that mediate inflammation and the 16HBE cell line is a common cell line used to study COPD pathogenesis in vitro . When exposed to harmful substances, such as cigarette smoke, airway epithelial cells are induced to produce various inflammatory cytokines (e.g., IL-18) leading to the recruitment of inflammatory cells (e.g., neutrophils) ( 43 ). In vitro and in vivo studies have demonstrated that smoking causes inflammation and cell death in lung tissue and airway cells ( 38 , 41 ).…”

Section: Discussionmentioning

confidence: 99%

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

Zhang

Chen

et al. 2022

Mol Med Rep

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Section: Discussionmentioning

confidence: 99%

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

Zhang

Chen

et al. 2022

Mol Med Rep

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“…Methionine sulfoxidation was the most frequent modification, especially in PMA-and LPS-induced NETs and MPO was the more extensively modified protein. As different stimuli can affect the protein composition and post-translational modifications involved in NET formation, it is likely that NETs induced under different stimuli may have different biological functions [29,[34][35][36].…”

Section: Neutrophilsmentioning

confidence: 99%

“…Additionally, raised blood neutrophil counts have been correlated with exacerbation frequency and mortality in patients with COPD [6]. Alongside chronic neutrophilic inflammation, NETs have also been found in the airways of both stable and exacerbating patients with COPD [60] and in murine models have been shown to be induced by cigarette smoke [35]. A study of 99 subjects with COPD found that sputum NETs, measured by immunoassay, were associated with exacerbation frequency and reduction in forced expiratory volume in 1 s (FEV 1 ) [61].…”

Section: Copdmentioning

confidence: 99%

Neutrophil extracellular traps in chronic lung disease: implications for pathogenesis and therapy

Keir

Chalmers

2022

Eur Respir Rev

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Neutrophilic inflammation has a key role in the pathophysiology of multiple chronic lung diseases. The formation of neutrophil extracellular traps (NETs) has emerged as a key mechanism of disease in neutrophilic lung diseases including asthma, COPD, cystic fibrosis and, most recently, bronchiectasis. NETs are large, web-like structures composed of DNA and anti-microbial proteins that are able to bind pathogens, prevent microbial dissemination and degrade bacterial virulence factors. The release of excess concentrations of proteases, antimicrobial proteins, DNA and histones, however, also leads to tissue damage, impaired mucociliary clearance, impaired bacterial killing and increased inflammation. A number of studies have linked airway NET formation with greater disease severity, increased exacerbations and overall worse disease outcomes across the spectrum of airway diseases. Treating neutrophilic inflammation has been challenging in chronic lung disease because of the delicate balance between reducing inflammation and increasing the risk of infections through immunosuppression. Novel approaches to suppressing NET formation or the associated inflammation are in development and represent an important therapeutic target. This review will discuss the relationship between NETs and the pathophysiology of cystic fibrosis, asthma, COPD and bronchiectasis, and explore the current and future development of NET-targeting therapies.

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“…Further, various neutrophil chemotractants were induced, explaining observations of high levels of neutrophils in COVID-19. In severe COVID-19, the levels of neutrophils are further higher as well as these neutrophils were shown to release chromatin, microbial proteins and oxidative enzymes resulting in formation of structures called neutrophil extracellular traps (NETs), which may contribute to respiratory failure ( 23 ). A transcriptomic signature of elevated proinflammatory genes including CXCL10, MCP1, MIP1A, MIP1B in BAL of COVID-19 patients has been confirmed by others ( 24 ).…”

Section: Introductionmentioning

confidence: 99%

Immune Correlates of COVID-19 Control

Poonia

Kottilil

2020

Front. Immunol.

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COVID-19 caused by SARS CoV2 emerged in China at the end of 2019 and soon become a pandemic. Since the virus is novel, pre-existing CoV2-specific immunity is not expected to exist in humans, although studies have shown presence of CoV2 cross-reactive T cells in unexposed individuals. Lack of effective immunity in most individuals along with high infectiousness of the virus has resulted in massive global public health emergency. Intense efforts are on to study viral pathogenesis and immune response to help guide prophylactic and therapeutic interventions as well as epidemiological assessments like transmission modeling. To develop an effective vaccine or biologic therapeutic, it is critical to understand the immune correlates of COVID-19 control. At the same time, whether immunity in recovered individuals is effective for preventing re-infection will be important for informing interventions like social distancing. Key questions that are being investigated regarding immune response in COVID-19 which will help these efforts include, investigations of immune response that distinguishes patients with severe versus mild infection or those that recover relative to those that succumb, durability of immunity in recovered patients and relevance of developed immunity in a cured patient for protection against re-infection as well as value of convalescent plasma from recovered patients as a potential therapeutic modality. This is a broad and rapidly evolving area and multiple reports on status of innate and adaptive immunity against SARS-CoV2 are emerging on a daily basis. While many questions remain unanswered for now, the purpose of this focused review is to summarize the current understanding regarding immune correlates of COVID-19 severity and resolution in order to assist researchers in the field to pursue new directions in prevention and control.

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Neutrophil extracellular traps induced by cigarette smoke contribute to airway inflammation in mice

Cited by 26 publications

References 36 publications

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

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

Neutrophil extracellular traps in chronic lung disease: implications for pathogenesis and therapy

Immune Correlates of COVID-19 Control

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