Leukocyte Function in Asthma and COPD
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|ClinicalTrials.gov Identifier: NCT00147069|
Recruitment Status : Completed
First Posted : September 7, 2005
Results First Posted : December 5, 2019
Last Update Posted : December 5, 2019
The aim of this study is to examine the inflammatory mechanisms involved in the pathogenesis of inflammatory lung disease, in particular to compare the inflammatory profile seen in asthma and COPD. Evidence for inflammation in asthma and COPD is based on the finding of increased numbers of macrophages and neutrophils in the lungs and respiratory secretions of these patients. The inflammatory cells produce proteases, as well as, reactive oxidant species resulting in a protease/anti-protease imbalance which favours lung destruction. The aim is to examine the inflammatory mediators released by inflammatory cells (such as, macrophages and lymphocytes) in order to determine whether there are differences between non-smoking subjects, smoking subjects and patients with asthma or COPD. Monocytes are precursors of alveolar macrophages, and both monocytes and neutrophils are recruited to the lung from the blood via the action of specific chemoattractants. We have evidence that in inflammation there are higher levels of these chemoattractants. Therefore these cells might also demonstrate the same changes seen in alveolar macrophages from these patients.
We also aim to assess the role of the macrophage precursor (monocyte) and neutrophils in the blood. We will also assess lymphocyte/monocyte interaction. We will do this as the lymphocyte may be involved in the initial recruitment of inflammatory cells. We will also assess the role of cytokines involved with monocyte/macrophage/neutrophil migration in induced sputum as well as the role of induced sputum in the migration of monocytes and neutrophils into the lung. Our aim is to link the initial changes in blood to the changes causing disease in the lungs. We aim to examine cellular responses in four groups of subjects, namely (i) non-smoking controls, (ii) smokers without clinical evidence of COPD or asthma, (iii) smokers with COPD (iv) asthmatic patients.
|Condition or disease|
|Asthma COPD Emphysema Chronic Bronchitis|
|Study Type :||Observational|
|Actual Enrollment :||60 participants|
|Official Title:||Investigation Into Inflammatory Mechanisms in Airway Cells in Smokers and Non-smokers With Inflammatory Lung Disease.|
|Actual Study Start Date :||April 2004|
|Actual Primary Completion Date :||April 2007|
|Actual Study Completion Date :||April 2007|
Non-smoking control subjects without lung disease
Non-smokers patients with asthma
Current smokers without airways obstruction, FEV1 >80% predicted
Patients with COPD and cigarette smokers
- Total Number of Inflammatory Cells Recovered in Sputum [ Time Frame: 1 year ]Sputum was induced via inhalation of hypertonic saline as previously described, and was processed for differential counts of inflammatory cells.
- Number of Matrix Metalloproteases (MMPs) MMP1 [ Time Frame: 1 year ]MMPs determined using paired antibody quantitative ELISAs
- Number of Matrix Metalloproteases (MMPs) MMP3 [ Time Frame: 1 year ]MMPs determined using paired antibody quantitative ELISAs
- Number of Matrix Metalloproteases (MMPs) MMP8 [ Time Frame: 1 year ]MMPs determined using paired antibody quantitative ELISAs
Biospecimen Retention: Samples Without DNA
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00147069
|Royal Brompton Hospital/NHLI Imperial College London|
|London, United Kingdom, SW3 6LY|
|Principal Investigator:||Louise E Donnelly, PhD||Imperial College London|