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Chronic Obstructive Pulmonary Disease (COPD) is a worldwide threat. Cigarette smoke (CS) exposure causes cardiopulmonary disease, COPD and increases the risk for pulmonary tumors. In addition to poor lung function, those with COPD are susceptible to bouts of dangerous inflammation triggered by pollutants or infection. These severe inflammatory episodes can lead to additional exacerbations, hospitalization, further deterioration of lung function and reduced survival. Suitable models of the inflammatory conditions associated with CS, which potentiate the downward spiral in COPD patients, are lacking and the underlying mechanisms that trigger exacerbations are not well understood. While initial CS exposure activates a protective role for vascular endothelial growth factor (VEGF) functions in barrier integrity, chronic exposure depletes pulmonary VEGF guard function in severe COPD. Thus, we hypothesized that mice with compromised VEGF production and challenged with CS would trigger human-like severe inflammatory progressions of COPD. In this model, we discovered that CS exposure promotes an amplified Interleukin-33 (IL-33) cytokine response and severe disease progression. Our VEGF knockout model combined with CS recapitulates severe COPD with an influx of IL-33-expressing macrophages and neutrophils. Normally, IL-33 is quickly inactivated by a post-translational disulfide bond (DSB) formation. Our results reveal that bronchoalveolar lavage fluid (BALF) from the CS-exposed, VEGF-deficient cohort promotes a significantly prolonged lifetime of active pro-inflammatory IL-33. Taken together, our data demonstrate that with the loss of a VEGF-mediated protective barrier, the CS response switches from a localized danger to an uncontrolled long-term and long-range amplified IL-33-mediated inflammatory response that ultimately destroys lung function.
This article was published in the following journal.
Name: American journal of respiratory cell and molecular biology
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Statistical formulations or analyses which, when applied to data and found to fit the data, are then used to verify the assumptions and parameters used in the analysis. Examples of statistical models are the linear model, binomial model, polynomial model, two-parameter model, etc.
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A cytochrome P-450 monooxygenase that can be induced by polycyclic aromatic xenobiotics in the liver of human and several animal species. This enzyme is of significant clinical interest due to the large number of drug interactions associated with its induction and its metabolism of THEOPHYLLINE. Caffeine is considered to be a model substrate for this enzyme. CYP1A2 activity can also be increased by environmental factors such as cigarette smoking, charbroiled meat, cruciferous vegetables, and a number of drugs including phenytoin, phenobarbital, and omeprazole.
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Prohibition against tobacco smoking in specific areas to control TOBACCO SMOKE POLLUTION.
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COPD (chronic obstructive pulmonary disease)
COPD (chronic obstructive pulmonary disease) is used for a number of conditions including chronic bronchitis and emphysema, which all lead to the airways in the lungs becoming damaged and thus narrower, making inhalation and exhalation harder...