https://search.dev.ndltd.org/etd/creighton/oai:cdr.creighton.edu:10504/29624
type: CreativeWork
name: Effect of Cigarette Smoke Exposure on Bronchial Hyperresponsiveness in Mice and Response to a Corticosteroid and/or a β2-Adrenergic Agonist and Effect of Cigarette Smoke Extract on Cytokines Release from U937 Cells.
description: The number of people affected with chronic inflammatory diseases of airways such as asthma and chronic obstructive pulmonary disease (COPD) are growing globally. Asthma is characterized by inflammation driven mainly by eosinophils, reversible airflow obstruction and significant airway hyperesponsiveness to airway stimuli like methacholine (MCh). It is increasingly prevalent in the US (24.6 million in 2009), particularly among children and some minority groups. Three hundred million people worldwide have been reported to have asthma with 250,000 annual deaths attributed to it. COPD is a pulmonary disease with irreversible airway obstruction and inflammation driven by neutrophils and macrophages. In the US in 2005, an estimated 126,000 US deaths were attributed to COPD. |Corticosteroids and/or β2 adrenergic agents are the main line of therapy for both asthma and COPD. However, some people with asthma, and the majority with COPD show diminished response to corticosteroid therapy. Various factors such as an increase in number of glucocorticoid receptors β, increase in activator protein-1 (AP-1), and increase in Th-2 cytokines (IL-4 and IL-13), and diminished histone deacetylase-2 activity are attributed to corticosteroid resistance. Since smoking is the primary risk factor of COPD and most of the patients with COPD show poor response to corticosteroids, oxidative stress should play an important role in causing diminished response to corticosteroids. In addition, various clinical studies have reported that people with asthma who are active smokers show less improvement in lung function with corticosteroids compared to non-smokers.|Based upon these rationales, we wanted to develop a model of smoking and COPD in mice and to study response to inhaled corticosteroid (ICS) and/or long acting beta agonists (LABA) as measured by bronchial hyperresponsiveness (BHR) to MCh and airway inflammation. We designed a 4 weeks smoke exposure study and administered inhaled fluticasone pro…
abstract: The number of people affected with chronic inflammatory diseases of airways such as asthma and chronic obstructive pulmonary disease (COPD) are growing globally. Asthma is characterized by inflammation driven mainly by eosinophils, reversible airflow obstruction and significant airway hyperesponsiveness to airway stimuli like methacholine (MCh). It is increasingly prevalent in the US (24.6 million in 2009), particularly among children and some minority groups. Three hundred million people worldwide have been reported to have asthma with 250,000 annual deaths attributed to it. COPD is a pulmonary disease with irreversible airway obstruction and inflammation driven by neutrophils and macrophages. In the US in 2005, an estimated 126,000 US deaths were attributed to COPD. |Corticosteroids and/or β2 adrenergic agents are the main line of therapy for both asthma and COPD. However, some people with asthma, and the majority with COPD show diminished response to corticosteroid therapy. Various factors such as an increase in number of glucocorticoid receptors β, increase in activator protein-1 (AP-1), and increase in Th-2 cytokines (IL-4 and IL-13), and diminished histone deacetylase-2 activity are attributed to corticosteroid resistance. Since smoking is the primary risk factor of COPD and most of the patients with COPD show poor response to corticosteroids, oxidative stress should play an important role in causing diminished response to corticosteroids. In addition, various clinical studies have reported that people with asthma who are active smokers show less improvement in lung function with corticosteroids compared to non-smokers.|Based upon these rationales, we wanted to develop a model of smoking and COPD in mice and to study response to inhaled corticosteroid (ICS) and/or long acting beta agonists (LABA) as measured by bronchial hyperresponsiveness (BHR) to MCh and airway inflammation. We designed a 4 weeks smoke exposure study and administered inhaled fluticasone pro…
author: Sapkota, Kiran
language: en_US
date published: 2012-05-31
date modified: 2026-07-24T01:51:08Z
provider: Creighton University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Creighton University

PropertyValue
property ID: Handle
value: http://hdl.handle.net/10504/29624