Ignite Creation Date:
2024-05-05 @ 4:39 PM
Last Modification Date:
2024-10-26 @ 9:22 AM
Study NCT ID:
NCT00281203
Status:
COMPLETED
Last Update Posted:
2013-07-16
First Post:
2006-01-20
Brief Title:
Comparison of Alveolar Macrophages in Healthy Individuals Versus Individuals With COPD
Sponsor:
University of Michigan
Organization:
University of Michigan
Study Overview
Official Title:
Innate and Adaptive Immunity in COPD Exacerbations Bronchoscopies on Healthy Volunteers
Status:
COMPLETED
Status Verified Date:
2013-07
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
This study group forms the normal subject control group in an experiment designed to determine whether the alveolar macrophages AMø of patients with chronic obstructive pulmonary disease COPD show abnormal responsiveness to bacterial and viral products Specifically the study will determine the dose-response characteristics of AMø for production of interleukin IL-6 IL-18 and IL-23 pro-inflammatory cytokines on stimulation by purified lipopolysaccharide a synthetic lipopeptide PAM3-Cys or poly IC These stimuli mimic the response to Gram-negative bacteria Gram-positive bacteria and RNA viruses respectively Results of the AMø from these healthy volunteers will be compared with AMø of COPD patients and smokers or ex-smokers with normal pulmonary function those samples are being obtained during clinically indicated bronchoscopies under a separate consent form
Detailed Description:
BACKGROUND
COPD is one of the most pressing healthcare problems facing our nation Acute exacerbations of COPD AE-COPD are 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
Bronchoscopies will be performed on healthy volunteers Subjects are reimbursed 30 for the initial visit and 150 at completion of the bronchoscopy to help defray travel expenses and for the time spent participating as a volunteer
COPD is one of the most pressing healthcare problems facing our nation Acute exacerbations of COPD AE-COPD are 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
Bronchoscopies will be performed on healthy volunteers Subjects are reimbursed 30 for the initial visit and 150 at completion of the bronchoscopy to help defray travel expenses and for the time spent participating as a volunteer
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| R01HL082480 | NIH | None | httpsreporternihgovquickSearchR01HL082480 |