Determinants of susceptibility to cigarette smoke. Potential roles for neuroendocrine cells and neuropeptides in airway inflammation, airway wall remodeling, and chronic airflow obstruction.

1994 ◽  
Vol 149 (6) ◽  
pp. 1692-1698 ◽  
Author(s):  
S M Aguayo
Keyword(s):  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Airflow Obstruction ◽  
Neuroendocrine Cells ◽  
Airway Wall

scholarly journals Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

2020 ◽  
Author(s):  
Yiping Ma ◽  
Zhu Li ◽  
Yalei Zhao ◽  
Mo Sun ◽  
Wuzhuang Sun ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cigarette Smoke ◽  
Rat Model ◽  
Airflow Obstruction ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Airway Wall ◽  
Tgf Β1

AbstractBackgroundRecently, some researchers have reported that PIgR expression is down-regulated in Chronic Obstructive Pulmonary Disease (COPD) and SIgA deficiency correlates with severity of airflow obstruction. What’ s more, some studies have demonstrated that 2 percent of hydrogen or hydrogen water is effective in treating and preventing various diseases.ObjectivesThe aim of this study was to observe the effect of hydrogen on the expression of SIgA, PIgR, IL-4, IL-5, TGF-β1 and IL-40 in lung tissue of COPD rats, to study the relationship between lung pathology parameter and SIgA, PIgR, therefore we can understand the effect of hydrogen on the development of COPD by changing SIgA expression of airway mucosal in COPD rats.MethodsA rat model of COPD was established by cigarette smoke exposure, and different concentrations of hydrogen were inhaled as intervention measures. After 4 months of cigarette smoke exposure, pathologic changes and airway wall remodeling of the lung were assessed by optical microscope. The protein expressions of SIgA, PIgR, IL-4, IL-5, TGF-β1 as well as IL-40 in the lung tissues were observed by immunohistochemistry or Western blot. The correlation between lung pathology parameter and the expression of SIgA, PIgR was analyzed. The correlation between SIgA and the expression of IL-4, IL-5, TGF-β1 and IL-40 was analyzed.ResultsThe results showed that hydrogen inhalation significantly ameliorated lung pathology and airway wall remodeling, increased the protein expression of SIgA, PIgR, IL-4, IL-5, and IL-40, and reduced the protein expression of TGF-β1.ConclusionsInhalation of 22% and 41.6% hydrogen showed a better effect than inhalation of 2% hydrogen. Hydrogen inhalation can significantly improve the expression of SIgA on the mucosal surface of COPD rats, which may be one of the mechanisms which hydrogen works on COPD pathogenesis.

scholarly journals FSTL1 aggravates cigarette smoke-induced airway inflammation and airway remodeling by regulating autophagy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Liu ◽  
Jiawei Xu ◽  
Tian Liu ◽  
Jinxiang Wu ◽  
Jiping Zhao ◽  
...  
Keyword(s):  
Lung Function ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Airway Remodeling ◽  
Critical Factor ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Impaired Lung Function

Abstract Background Cigarette smoke (CS) is a major risk factor for Chronic Obstructive Pulmonary Disease (COPD). Follistatin-like protein 1 (FSTL1), a critical factor during embryogenesis particularly in respiratory lung development, is a novel mediator related to inflammation and tissue remodeling. We tried to investigate the role of FSTL1 in CS-induced autophagy dysregulation, airway inflammation and remodeling. Methods Serum and lung specimens were obtained from COPD patients and controls. Adult female wild-type (WT) mice, FSTL1± mice and FSTL1flox/+ mice were exposed to room air or chronic CS. Additionally, 3-methyladenine (3-MA), an inhibitor of autophagy, was applied in CS-exposed WT mice. The lung tissues and serum from patients and murine models were tested for FSTL1 and autophagy-associated protein expression by ELISA, western blotting and immunohistochemical. Autophagosome were observed using electron microscope technology. LTB4, IL-8 and TNF-α in bronchoalveolar lavage fluid of mice were examined using ELISA. Airway remodeling and lung function were also assessed. Results Both FSTL1 and autophagy biomarkers increased in COPD patients and CS-exposed WT mice. Autophagy activation was upregulated in CS-exposed mice accompanied by airway remodeling and airway inflammation. FSTL1± mice showed a lower level of CS-induced autophagy compared with the control mice. FSTL1± mice can also resist CS-induced inflammatory response, airway remodeling and impaired lung function. CS-exposed WT mice with 3-MA pretreatment have a similar manifestation with CS-exposed FSTL1± mice. Conclusions FSTL1 promotes CS-induced COPD by modulating autophagy, therefore targeting FSTL1 and autophagy may shed light on treating cigarette smoke-induced COPD.

Asthma with Irreversible Airway Obstruction in Smokers and Nonsmokers: Links between Airway Inflammation and Structural Changes

Respiration ◽  
2020 ◽  
pp. 1-11
Author(s):  
Louis-Philippe Boulet ◽  
Marie-Eve Boulay ◽  
Harvey O. Coxson ◽  
Cameron J. Hague ◽  
Joanne Milot ◽  
...  
Keyword(s):  
Lung Function ◽  
Airway Obstruction ◽  
Airway Inflammation ◽  
Wall Thickness ◽  
Structural Changes ◽  
Smoking History ◽  
Airway Wall ◽  
Tobacco Exposure ◽  
Airway Wall Thickness ◽  
Irreversible Airway Obstruction

<b><i>Background:</i></b> The development of irreversible airway obstruction (IRAO) in asthma is related to lung/airway inflammatory and structural changes whose characteristics are likely influenced by exposure to tobacco smoke. <b><i>Objective:</i></b> To investigate the interplay between airway and lung structural changes, airway inflammation, and smoking exposure in asthmatics with IRAO. <b><i>Methods:</i></b> We studied asthmatics with IRAO who were further classified according to their smoking history, those with ≥20 pack-years of tobacco exposure (asthmatics with smoking-related IRAO [AwS-IRAO]) and those with &#x3c;5 pack-years of tobacco exposure (asthmatics with nonsmoking-related IRAO [AwNS-IRAO]). In addition to recording baseline clinical and lung function features, all patients had a chest computed tomography (CT) from which airway wall thickness was measured and quantitative and qualitative assessment of emphysema was performed. The airway inflammatory profile was documented from differential inflammatory cell counts on induced sputum. <b><i>Results:</i></b> Ninety patients were recruited (57 AwS-IRAO and 33 AwNS-IRAO). There were no statistically significant differences in the extent of emphysema and gas trapping between groups on quantitative chest CT analysis, although Pi10, a marker of airway wall thickness, was significantly higher in AwS-IRAO (<i>p</i> = 0.0242). Visual analysis showed a higher prevalence of emphysema (<i>p</i> = 0.0001) and higher emphysema score (<i>p</i> &#x3c; 0.0001) in AwS-IRAO compared to AwNS-IRAO and distribution of emphysema was different between groups. Correlations between radiological features and lung function were stronger in AwS-IRAO. In a subgroup analysis, we found a correlation between airway neutrophilia and emphysematous features in AwS-IRAO and between eosinophilia and both airway wall thickness and emphysematous changes in AwNS-IRAO. <b><i>Conclusions:</i></b> Although bronchial structural changes were relatively similar in smoking and nonsmoking patients with asthma and IRAO, emphysematous changes were more predominant in smokers. However, neutrophils in AwS-IRAO and eosinophils in AwNS-IRAO were associated with lung and airway structural changes.

scholarly journals Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia syndrome

2016 ◽  
Vol 47 (6) ◽  
pp. 1829-1841 ◽  
Author(s):  
Giulio Rossi ◽  
Alberto Cavazza ◽  
Paolo Spagnolo ◽  
Nicola Sverzellati ◽  
Lucia Longo ◽  
...  
Keyword(s):  
Lung Biopsy ◽  
Airflow Obstruction ◽  
Neuroendocrine Cells ◽  
Neuroendocrine Cell ◽  
World Health ◽  
Cell Hyperplasia ◽  
Carcinoid Tumours ◽  
Neoplastic Lesion ◽  
Asymptomatic Patients ◽  
Pulmonary Neuroendocrine Cell

The term diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) may be used to describe a clinico-pathological syndrome, as well as an incidental finding on histological examination, although there are obvious differences between these two scenarios. According to the World Health Organization, the definition of DIPNECH is purely histological. However, DIPNECH encompasses symptomatic patients with airway disease, as well as asymptomatic patients with neuroendocrine cell hyperplasia associated with multiple tumourlets/carcinoid tumours. DIPNECH is also considered a pre-neoplastic lesion in the spectrum of pulmonary neuroendocrine tumours, because it is commonly found in patients with peripheral carcinoid tumours.In this review, we summarise clinical, physiological, radiological and histological features of DIPNECH and critically discuss recently proposed diagnostic criteria. In addition, we propose that the term “DIPNECH syndrome” be used to indicate a sufficiently distinct patient subgroup characterised by respiratory symptoms, airflow obstruction, mosaic attenuation with air trapping on chest imaging and constrictive obliterative bronchiolitis, often with nodular proliferation of neuroendocrine cells with/without tumourlets/carcinoid tumours on histology. Surgical lung biopsy is the diagnostic gold standard. However, in the appropriate clinical and radiological setting, transbronchial lung biopsy may also allow a confident diagnosis of DIPNECH syndrome.

Relationship of pulmonary arterial pressure and airflow obstruction to emphysema

1993 ◽  
Vol 74 (3) ◽  
pp. 1320-1324 ◽  
Author(s):  
J. L. Wright
Keyword(s):  
Arterial Pressure ◽  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Pulmonary Arterial Pressure ◽  
Airflow Obstruction ◽  
Control Group ◽  
Moderate Degree ◽  
Emphysematous Lung ◽  
Pulmonary Arterial ◽  
Relationship Of

Guinea pigs were exposed to cigarette smoke for 6 mo, after which lung and cardiac function and lung morphology were examined. The smoke-exposed animals were divided into two groups on the basis of final pulmonary arterial pressure. We found that the smoke-exposed animals with increased pulmonary arterial pressure had a moderate degree of airflow obstruction compared with the normotensive smoke group, which showed only mild airflow obstruction, and with the control group. Both smoke groups had similar degrees of emphysema. Although both smoke groups had an increased percentage of muscularized small arterioles, only the group with increased pulmonary arterial pressure had an altered flow-pressure response to dobutamine. We conclude that although cigarette smoke appears to induce changes in the vascular structure and to produce emphysematous lung destruction, the increased pulmonary arterial pressure in guinea pigs chronically exposed to smoke is not directly related to either of these findings. Instead, it appears that there is a dynamic alteration of both the airways, producing airflow obstruction, and the vasculature, producing increased pulmonary arterial pressure.

scholarly journals Corrigendum: Autophagy Promotes Cigarette Smoke-Initiated and Elastin-Driven Bronchitis-Like Airway Inflammation in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Hua-Qiong Huang ◽  
Na Li ◽  
Dan-Yang Li ◽  
Du Jing ◽  
Zheng-Yuan Liu ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Cigarette Smoke

scholarly journals Role of Neuro‐immune Interactions in a Cigarette Smoke‐induced Chronic Airway Inflammation Mouse Model

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Kata Csekő ◽  
István Szitter ◽  
Zsófia Hajna ◽  
Krisztián Elekes ◽  
Ágnes Kemény ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Chronic Airway

scholarly journals Induction of fibrogenic mediators by fine and ultrafine titanium dioxide in rat tracheal explants

1999 ◽  
Vol 277 (5) ◽  
pp. L975-L982 ◽  
Author(s):  
A. Churg ◽  
B. Gilks ◽  
J. Dai
Keyword(s):  
Gene Expression ◽  
Titanium Dioxide ◽  
Growth Factor ◽  
Ultrafine Particles ◽  
Transforming Growth Factor ◽  
Airflow Obstruction ◽  
Pdgf Receptor ◽  
Airway Wall ◽  
Transforming Growth Factor Α ◽  
Tracheal Explants

Respirable ambient particles [particulate matter <10 μm (PM10)] are associated with both acute and chronic adverse health effects including chronic airflow obstruction. PM10 can induce expression of inflammatory and fibrogenic mediators, but there is controversy about the types and/or sizes of particles involved and, in particular, whether ultrafine particles are the major toxic agents. To examine whether particle size affects mediator generation, we exposed rat tracheal explants, an inflammatory cell-free model of the airway wall, to various concentrations up to 500 μg/cm2 of fine (0.12 μm) or ultrafine (0.021 μm) titanium dioxide (anatase), maintained the explants in an organ culture in air for 1–7 days, and used RT-PCR to examine the expression of fibrogenic mediators and procollagen. No increase in gene expression was seen at 1 or 3 days, but at 5 days, ultrafine dust induced a small increase in procollagen. At 7 days, fine titanium dioxide produced significantly greater increases for platelet-derived growth factor (PDGF)-B, transforming growth factor-α, and transforming growth factor-β compared with those by ultrafine dust; both dusts produced similar increases for PDGF-A; and ultrafine dust produced increases in procollagen expression, whereas fine dust had no effect. Expression levels were dose related. Both dusts produced a similar decrease in expression of PDGF receptor-α and a similar increase in PDGF receptor-β. These observations suggest that ultrafine particles are intrinsically able to induce procollagen expression even in the absence of inflammatory cells; that chronic exposure to PM10 may result in chronic airflow obstruction, in part because of ultrafine particle-mediated increases in airway wall fibrosis; and that chemically identical dusts of differing size can produce quite different patterns of gene expression in the airway wall. Differential upregulation of PDGF receptors does not appear to explain dust-induced fibrosis in this model.

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