View Clinical Trial (Medical Research Study)
Innate and Adaptive Immunity in COPD Exacerbations: Surgical Volunteers
| City: |
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Ann Arbor |
| State: |
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Michigan |
| Zip Code: |
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48105 |
| Conditions: |
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Pulmonary Disease, Chronic Obstructive - Lung Diseases, Obstructive |
| Purpose: |
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The purpose of this study is to determine whether the lungs of individuals with chronic
obstructive pulmonary disease (COPD) contain resident memory T lymphocytes that can produce
a combination of cytokines that induce the symptoms of an acute exacerbation of COPD
(AE-COPD). Specifically, the study will determine cell-surface receptors of lung T cells
in comparison with blood T cells from the same subject, and will examine anti-CD3-activated
blood or lung T cells for interleukin (IL)-6 and interferon-gamma production in response to
IL-18, and for IL-17A production in response to recombinant IL-23.
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| Study Summary: |
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BACKGROUND:
COPD is one of the most pressing healthcare problems facing our nation. AE-COPD is
responsible for the bulk of healthcare costs, and much of the morbidity and decline in
health status among individuals with this common disease. The lack of accepted animal
models of AE-COPD necessitates novel approaches using human samples. Advances in the
understanding of the pathogenesis have been slowed, in part, due to controversy as to how
exacerbations should be defined. The prevailing paradigm has defined AE-COPD as
event-based. Such definitions clearly identify groups of patients with accelerated loss of
pulmonary function and increased mortality. However, limited data show that symptom-based
definitions of AE-COPD also capture episodes inducing significant morbidity and functional
decline, and hence of concern to patients. Fundamental mechanisms are lacking to explain
AE-COPD defined by either means.
Controversy also surrounds triggers of AE-COPD. Bacteria and viruses are involved in some
episodes, but the relative importance of each is intertwined with disputes over the
definition of AE-COPD. Progress at linking specific pathogens to molecular pathogenesis has
been slow, both due to their diversity, and to the high rates of bacterial colonization of
patients with COPD, even in the stable state. Moreover, in many AE-COPD cases, no pathogen
can be identified. Without negating the value of analyzing infections with specific
species of pathogens, it appears that progress in molecular pathogenesis could be
accelerated by focusing on unifying features of the pulmonary immune response during
AE-COPD.
DESIGN NARRATIVE:
The research protocol involves isolating lung lymphocytes from surgical specimens of
patients already undergoing clinically indicated lung resections. Surgical lung resections
may be performed either by open thoracotomy or by video-assisted thoracoscopic surgery
(VATS), and could include pneumonectomies, lobectomies, or wedge-excisions, as dictated by
clinical care of the patient. This protocol will exclusively use tissue that is of excess
after a clinical diagnosis is established. The setting is the operating rooms at the Ann
Arbor VA Hospital or the University of Michigan Hospital System. Subjects will be
recruited from the outpatient clinics, but will be inpatients at the time of surgery.
Subjects will not undergo any additional procedures beyond routine clinical care as a result
of participating in this protocol. However, it is anticipated that the study will have
access to the medical record to extract results of demographic data, including occupational
exposures and smoking history, pulmonary function testing, and results of imaging and other
staging studies.
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| Criteria: |
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Inclusion criteria:
- Diagnosis of COPD AND underwent lung resection for malignancy OR lung volume
reduction surgery OR lung transplantation OR lung resection for nodules and masses
Exclusion criteria:
- Mental incompetence or active psychiatric illness
- Currently using more than 20 mg/day of Prednisone
- Asthma as primary clinical pulmonary diagnosis
- Cystic fibrosis
- Clinically significant bronchiectasis
- Other inflammatory or fibrotic lung disease
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| NCT ID: |
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NCT00281229 |
| Primary Contact: |
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Study Chair
Jeffrey L. Curtis
University of Michigan at Ann Arbor
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| Backup Contact: |
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N/A |
| Location Contact: |
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Ann Arbor, Michigan 48105
United States
Christi Getty, RRT
Phone: 734-769-7100
Email: cgetty@med.umich.edu
Site Status: Recruiting |
| Data Source: |
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ClinicalTrials.gov |
| Date Processed: |
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June 19, 2013 |
| Modifications to this listing: |
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