|
Endotoxin and Bronchial Inflammation in Asthma Clinical Trials References presented on Clinical Trials Search isn't meant to be a substitute for proven healthcare advice, trips or professional assistance using a genuine physician. We are not docs. Always confer with your physician about Endotoxin and Bronchial Inflammation in Asthma conditions. Clinical Trials Search.org is a site devoted to listing clinical research studies in human subjects. Endotoxin and Bronchial Inflammation in Asthma Clinical research trials and Endotoxin and Bronchial Inflammation in Asthma healthcare trials happen in hundreds of localities throughout the United States of America. A clinical trial or clinical study is a research project with human volunteer subjects. Clinical drug trials and pharmaceutical clinical trials usually evaluate the potency of new drugs. The propose of the studies / projects is to answer particular human health questions. Clinical trials are a popular way for mDs, government agencies, and private sector companies to detect cures for all sorts of conditions, such as Endotoxin and Bronchial Inflammation in Asthma. Endotoxin and Bronchial Inflammation in Asthma Clinical Trials and other clinical trials allow volunteers to acquire healthcare treatment choices before they are available to the general public. Some times the subjects recieve professional assistance for free, and every now and again they are compensated for their time. Sometimes there is a cost for a Endotoxin and Bronchial Inflammation in Asthma clinical trial. Subjects frequently obtain the most expert healthcare possible for their Endotoxin and Bronchial Inflammation in Asthma condition. Risks are a reality, nevertheless, and can include more or frequent doctor trips, medical risks (possibly life-threatening), and/or the treatment being uneffective. Trials are federally governed with stern guidelines to protect clinical trials patients.
|
|
|
|
|
|
|
Home > "E" Clinical Trials Conditions > Endotoxin and Bronchial Inflammation in Asthma  Endotoxin and Bronchial Inflammation in Asthma
Endotoxin and Bronchial Inflammation in Asthma
For Condition: Lung Diseases,Asthma
Status: No longer recruiting
Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) ,
Synopsis: To evaluate airway inflammation in persons with asthma exposed to endotoxin, a common occupational air contaminant. Subjects are subsequently challenged with allergen.
Details: BACKGROUND: Endotoxin (or lipopolysaccharide [LPS]) is a potent inflammatory stimulant which is found in ambient air in occupational settings. Asthma in the workplace is an increasingly significant problem. Asthma is characterized by airway inflammation and increased reactivity to both allergic and non-allergic stimuli. LPS is known to induced airway inflammation in normal subjects and to enhance airway reactivity in asthmatics. Additionally, both alveolar macrophages and mononuclear cells from asthmatics secrete higher amounts of cytokines (interleukins 1 and 8 [IL-1, IL-8] and granulocyte macrophage-colony stimulating factor [GM-CSF] ) than those from normals. Thus, it is likely that LPS enhances allergen-induced inflammation and that allergic asthmatics are more sensitive to the effects of LPS. Preliminary data show that exposure to low levels (250 ng/m3) of LPS at risk for four hours enhances both immediate responsiveness to inhaled allergen and allergen-induced eosinophils as observed in induced sputum. In the nasal airways of allergics, a single dose of 1,000 nanograms of LPS enhances polymorphonuclear leukocyte influx associated with allergen challenge. This latter finding also correlates well with baseline IL-8 and ECP levels, suggesting that constitutive airway inflammation enhances response to these stimuli. DESIGN NARRATIVE: The effect of endotoxin LPS (5,000 nanograms) is compared on airway inflammation and methacholine response and lung function in normals and asthmatics; the effect of LPS (500 nanograms) is compared on allergen-induced reactivity and inflammatory cell influx following LPS exposure (5,000 nanograms) in asthmatics, likely as a result of decreasing baseline inflammation. To examine potential cellular mediation of the effect of LPS in asthma, cytokine secretion of mononuclear cells to LPS of subjects responding to LPS (or those in whom LPS enhance response to allergen) is compared to those who did not respond. In vitro monocyte and in vivo airway responses of asthmatics who are responsive and non-responsive is compared to baseline sputum and nasal lavage fluid IL-8 and ECP to determine if either in vitro monocyte responses or IL-8 and ECP in readily obtained airway fluids may serve as biomarkers of LPS responsiveness and might be used as a marker for a LPS-response phenotype in humans for future mechanistic and intervention studies. Finally, practical data on the effect of LPS in asthmatics (at levels found in typical work settings) and the ability of standard anti-inflammatory therapy to protect asthmatic workers unavoidable exposed to LPS will be obtained. The study was renewed in 2001 and continues through December, 2005.
Eligibility:
Study Type: Observational, Natural History, Defined Population
Minimum Age/Maximum Age: /
Genders: Male
Protocol Entry Criteria: No eligibility criteria
Total Enrollment:
Location and Contact Information:
Overall Study Official:
DavidPeden, , University of North Carolina
Additional Information:
Study ID Numbers: 5094;
Study Start Date: January 1999
Record last reviewed: February 2004
Additional information available at: clinicaltrials.gov
Clinicaltrials.gov Reference link: NCT00005550
Other Asthma Studies:
1. The Genetics of Environmental Asthma
2. Controlling Asthma at School
3. Community Organizing Network for Environmental Health
4. Genetics of Airway Responsiveness and Lung Function
5. Intervention for Hispanic Children with Asthma
Related Studies:
Other Asthma Clinical Trials
Other Clinical Trials
Other Clinical Trials
Endotoxin and Bronchial Inflammation in Asthma
|
|
|
|
|
|
|
|
