CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema

Shigeta, Ayako; Tada, Yuji; Wang, Ji‐Yang; Ishizaki, Shunsuke; Tsuyusaki, Junichi; Yamauchi, Keita; Kasahara, Yasunori; Iesato, K; Tanabe, Nobuhiro; Takiguchi, Yuichi; Sakamoto, Akemi; Tokuhisa, Takeshi; Shibuya, Kazutoshi; Hiroshima, Kenzo; West, James

doi:10.1152/ajplung.00337.2011

Cited by 13 publications

(10 citation statements)

References 42 publications

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“…The existing evidence regarding PM and sCD40L mainly focuses on cardiovascular disease [37]. However, some studies have indicated that sCD40L plays a contributing role in pulmonary emphysema [38].…”

Section: Discussionmentioning

confidence: 99%

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Gao

et al. 2020

Environ Health

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Background: Exposure to air pollution is associated with chronic obstructive pulmonary disease (COPD). However, findings on the effects of air pollution on lung function and systemic inflammation in Chinese COPD patients are inconsistent and scarce. This study aims to evaluate the effects of ambient air pollution on lung function parameters and serum cytokine levels in a COPD cohort in Beijing, China. Methods: We enrolled COPD participants on a rolling basis from December 2015 to September 2017 in Beijing, China. Follow-ups were performed every 3 months for each participant. Serum levels of 20 cytokines were detected every 6 months. Hourly ambient pollutant levels over the same periods were obtained from 35 monitoring stations across Beijing. Geocoded residential addresses of the participants were used to estimate daily mean pollution exposures. A linear mixed-effect model was applied to explore the effects of air pollutants on health in the first-year of follow-up. Results: A total of 84 COPD patients were enrolled at baseline. Of those, 75 COPD patients completed the first-year of follow-up. We found adverse cumulative effects of particulate matter less than 2.5 μm in aerodynamic diameter (PM 2.5), nitrogen dioxide (NO 2), sulfur dioxide (SO 2) and carbon monoxide (CO) on the forced vital capacity % predicted (FVC % pred) in patients with COPD. Further analyses illustrated that among COPD patients, air pollution exposure was associated with reduced levels of serum eotaxin, interleukin 4 (IL-4) and IL-13 and was correlated with increased serum IL-2, IL-12, IL-17A, interferon γ (IFNγ), monocyte displacing protein 1 (MCP-1) and soluble CD40 ligand (sCD40L). Conclusion: Acute exposures to PM 2.5 , NO 2 , SO 2 and CO were associated with a reduction in FVC % pred in COPD patients. Furthermore, short-term exposure to air pollutants increased systemic inflammation in COPD patients; this may be attributed to increased Th1 and Th17 cytokines and decreased Th2 cytokines.

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Section: Discussionmentioning

confidence: 99%

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Gao

et al. 2020

Environ Health

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“…This was in accordance with the well-known hypothesis that depleting vascular endothelial growth factor induces the apoptosis of parenchymal epithelial and endothelial cells and results in emphysematous changes in COPD. 26 – 29 In contrast, air way inflammation in asthma is accompanied by vascular endothelial growth factor oversecretion and an increase in subepithelial microvessels. 30 Leakage from these immature microvessels enhances airway inflammation and hypersensitivity.…”

Section: Discussionmentioning

confidence: 99%

Clinical, physiological, and radiological features of asthma–chronic obstructive pulmonary disease overlap syndrome

Suzuki

Tada

Kawata

et al. 2015

COPD

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BackgroundAsthma–chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) is associated with rapid decline in lung function, poorer health-related quality-of-life outcomes, and frequent exacerbations, compared to COPD alone. Although the numbers of patients with ACOS have increased, there is little established evidence regarding diagnostic criteria and treatment options. Thus, the aim of our study was to clarify the clinical, physiological, and radiological features of patients with ACOS.MethodsWe examined a total of 100 patients with COPD and 40 patients with ACOS, who were selected based on clinical criteria. All patients underwent baseline testing, including a COPD assessment test, pulmonary function tests, and multidetector row computed tomography imaging. Percentage of low attenuation volume, percentage of wall area, and percentage of total cross-sectional area of pulmonary vessels less than 5 mm2 (%CSA <5) were determined using multidetector row computed tomography. ACOS patients were administered a fixed dose of budesonide/formoterol (160/4.5 μg, two inhalations; twice daily) for 12 weeks, after which the ACOS patients underwent multidetector row computed tomography to measure the same parameters.ResultsAt baseline, the ACOS patients and COPD patients had a similar degree of airflow limitation, vital capacity, and residual volume. ACOS patients had higher COPD assessment test scores, percentage of wall area, and %CSA <5 than COPD patients. Compared to baseline, budesonide/formoterol treatment significantly increased the forced expiratory volume in 1 second and decreased the degree of airway wall thickness (percentage of wall area) as well as pulmonary microvascular density (%CSA <5) in ACOS patients.ConclusionOur results suggest that ACOS is characterized by an airway lesion–dominant phenotype, in contrast to COPD. Higher %CSA <5 might be a characteristic feature of ACOS.

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“…Accordingly, alveolar epithelial cell inflammation and apoptosis are significant mechanisms in the pathobiology of CS-induced COPD (23,110). The deleterious components of cigarette smoke recruit macrophages, neutrophils, and T lymphocytes, which, in turn, aggravate air space enlargement and alveolar destruction, culminating in emphysematous inflammation (23).…”

Section: Key Studies and Recent Advances: A Literature Review From 20mentioning

confidence: 99%

“…IFN-␥ may be a useful indicator of COPD severity and, through mechanisms relatively unknown, play a role in initiating the immune response during virus-induced exacerbation. However, most importantly, through the stimulation of CD40, an important TNF receptor, IFN-␥ has been thought to induce the Fas-apoptotic pathway in epithelial cells and stimulate the enlargement of emphysematous airways (110). In addition, extracellular adenosine is often increased during tissue injury and inflammatory insults by the stimulation of ectonucleotidases, CD39 and CD73, or by variations in the activity and expression of adenosine deaminase (76).…”

Section: Key Studies and Recent Advances: A Literature Review From 20mentioning

confidence: 99%

Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

Zuo

Sergakis

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

215

139

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Cigarette smoking (CS) can impact the immune system and induce pulmonary disorders such as chronic obstructive pulmonary disease (COPD), which is currently the fourth leading cause of chronic morbidity and mortality worldwide. Accordingly, the most significant risk factor associated with COPD is exposure to cigarette smoke. The purpose of the present study is to provide an updated overview of the literature regarding the effect of CS on the immune system and lungs, the mechanism of CS-induced COPD and oxidative stress, as well as the available and potential treatment options for CS-induced COPD. An extensive literature search was conducted on the PubMed/Medline databases to review current COPD treatment research, available in the English language, dating from 1976 to 2014. Studies have investigated the mechanism by which CS elicits detrimental effects on the immune system and pulmonary function through the use of human and animal subjects. A strong relationship among continued tobacco use, oxidative stress, and exacerbation of COPD symptoms is frequently observed in COPD subjects. In addition, therapeutic approaches emphasizing smoking cessation have been developed, incorporating counseling and nicotine replacement therapy. However, the inability to reverse COPD progression establishes the need for improved preventative and therapeutic strategies, such as a combination of intensive smoking cessation treatment and pharmaceutical therapy, focusing on immune homeostasis and redox balance. CS initiates a complex interplay between oxidative stress and the immune response in COPD. Therefore, multiple approaches such as smoking cessation, counseling, and pharmaceutical therapies targeting inflammation and oxidative stress are recommended for COPD treatment.

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CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema

Abstract: . CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema.

Cited by 13 publications

References 42 publications

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Clinical, physiological, and radiological features of asthma–chronic obstructive pulmonary disease overlap syndrome

Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

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CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema

Abstract: . CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema.

Cited by 13 publications

References 42 publications

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Clinical, physiological, and radiological features of&nbsp;asthma&ndash;chronic obstructive pulmonary disease&nbsp;overlap syndrome

Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

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Clinical, physiological, and radiological features of asthma–chronic obstructive pulmonary disease overlap syndrome