Neutrophil extracellular traps induced by cigarette smoke activate plasmacytoid dendritic cells

Qiu, Shilin; Zhang, Hui; Tang, Qin; Bai, Jing; Zhou, He; Zhang, Jianquan; Li, Meihua; Deng, Jingmin; Liu, Guangnan; Zhong, Xiaoning

doi:10.1136/thoraxjnl-2016-209887

Cited by 76 publications

(70 citation statements)

References 32 publications

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“…The analysis was performed to identify whether NET absorbance is a significant independent predictor of disease progression (overall stage) and adjusting for important available confounders: age, sex, BMI, smoking, diabetes, and comorbidities. All confounders were chosen because they have been shown to induce NET release (39,48,49). Multivariable logistic regression analyses were performed, and model assumptions were tested using graphical representations of residuals, residuals versus main predictor variable graphs, and residuals versus predicted variable graphs.…”

Section: Methodsmentioning

confidence: 99%

Primary tumors induce neutrophil extracellular traps with targetable metastasis-promoting effects

et al. 2019

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Section: Methodsmentioning

confidence: 99%

Primary tumors induce neutrophil extracellular traps with targetable metastasis-promoting effects

et al. 2019

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“…These structures were named NETs, and the peculiar cell death pathway was termed NETosis, accordingly [4]. A large number of inducers of NETosis have been described, including bacteria or bacterial components [1], fungi [5], protozoa [6, 7], viruses [8], activated platelets [9], complement-derived peptides [10], autoantibodies [11], IL-8 [1], hydrogen peroxide [12], urate crystals [13], cigarette smoke [14], and ionophores [15]. PMA-induced NETosis has been studied in some detail and a number of molecular events leading to NET formation have been identified.…”

Section: Structure and Generation Of Neutrophil Extracellular Trapsmentioning

confidence: 99%

“…After long-term exposure to inhaled irritants like tobacco smoke, COPD patients suffer from recurrent bacterial and viral infections leading to repeated exacerbations. Tobacco smoke has been found to directly induce NET formation [14], possibly due to its LPS content. Additionally, nicotine directly induces NETosis [65-67], and it is not surprising that NETs have been found in COPD lungs [68].…”

Section: Lung Diseasesmentioning

confidence: 99%

Neutrophil Extracellular Traps in the Second Decade

2018

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Nearly 15 years after the first description of neutrophil extracellular traps (NETs), our knowledge concerning this structure has expanded considerably. Initially, NETs were considered solely an elaborate function of the innate immune system to combat invading microorganisms. Successively it became clear that NETs have farther-reaching capabilities. They are involved in a series of pathophysiological mechanisms ranging from inflammation to thrombosis where they fulfill essential functions when produced at the right site and the right time but can have a serious impact when generation or clearance of NETs is inadequately controlled. This review provides a concise overview on the far-reaching functions of NETs in health and disease.

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“…Isolated neutrophils (1 × 10 6 neutrophils) were divided into three groups: For control conditions, the first group is cultured and treated with cultured medium without phorbol myristate acetate (PMA); the second group is cultured with PMA (100 nmol/L) as described previously, 22 and to analyse the ability of NET inhibitor to prevent NET release from stimulated neutrophils as described previously, 23 the third group is treated with diphenyleneiodonium chloride (DPI 10 μmol/L; Sigma-Aldrich) for 30 minutes and followed by PMA stimulation. After neutrophils in three groups were cultured for 3 hours respectively, medium was removed and adherent NETs were washed with prewarmed RPMI1640 (Lonza Walkersville Inc).…”

Section: Isolation Of Blood Neutrophils and In Vitro Induction Of Netmentioning

confidence: 99%

Neutrophil extracellular traps in nasal secretions of patients with stable and exacerbated chronic rhinosinusitis and their contribution to induce chemokine secretion and strengthen the epithelial barrier

Hwang

Kim

et al. 2019

Clin Experimental Allergy

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Background: Neutrophil extracellular traps (NETs) participate in innate immunity by trapping microorganisms. Their pathophysiological implications have not been defined in chronic rhinosinusitis (CRS). Objective: We investigated the presence of NETs in nasal secretion of patients with stable or exacerbated CRS and evaluated whether NETs participate in the secretion of chemokines in sinonasal epithelial cells, the epithelial permeability, and transendothelial leucocyte migration, and elucidate whether NETs are released by macrolides and dexamethasone. Methods: The presence of NETs in nasal secretion and the release of NETs from neutrophils stimulated with macrolides or dexamethasone were evaluated by dsDNA Assay kit and fluorescence microscope. The chemokine secretion, epithelial permeability, and transendothelial leucocyte migration were measured in cultured cells incubated with NETs, the supernatant of unstimulated neutrophils (unstim), NETs inhibitor (DPI), or H3Cit, where the expression of junctional complex proteins and ICAM-1 was evaluated by real-time PCR, Western blots, and confocal microscope. Results: The amount of NETs and NETs-forming neutrophils in nasal secretion increased in exacerbated CRS. Epithelial cells treated with NETs or H3Cit secreted chemokines and showed decreased permeability associated with up-regulated junctional complex proteins. Increased transendothelial leucocyte migration associated with up-regulated ICAM-1 was noted in endothelial cells treated with NETs or H3Cit.These findings were not found in cells treated with unstim, or DPI. NETs were released by macrolides, but not by dexamethasone. Conclusions and Clinical Relevance: NETs formation increased in exacerbated CRS,inducing chemokine secretion, strengthening the epithelial barrier, and promoting the neutrophils infiltration. Therefore, the release of NETs in CRS might be beneficial or detrimental to CRS patients. K E Y W O R D Schemokines, dexamethasone, epithelial permeability, macrolides, neutrophil extracellular traps, transendothelial leucocyte migration

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Neutrophil extracellular traps induced by cigarette smoke activate plasmacytoid dendritic cells

Cited by 76 publications

References 32 publications

Primary tumors induce neutrophil extracellular traps with targetable metastasis-promoting effects

Primary tumors induce neutrophil extracellular traps with targetable metastasis-promoting effects

Neutrophil Extracellular Traps in the Second Decade

Neutrophil extracellular traps in nasal secretions of patients with stable and exacerbated chronic rhinosinusitis and their contribution to induce chemokine secretion and strengthen the epithelial barrier

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