Immunosuppressive Effects of Smoking and HIV-1 on the Development of Lung Disease
This study plans to learn more about pulmonary complications of HIV/AIDS. Even though antiretroviral therapy (ART) has dramatically decreased the number of opportunistic infections and deaths in HIV infected patients, pulmonary complications (including chronic obstructive pulmonary disease [COPD] development and pneumonias resulting in decreased lung function) of HIV/AIDS continue to be a major cause of morbidity and mortality in this population. The mechanisms underlying the increased risk of COPD and decreased lung function in HIV infected individuals is not well understand and needs to be studied.
We hypothesize that the immunoregulatory consequences and immunosuppressive lung milieu secondary to HIV and cigarette smoke combine to increase the risk of lung infection and injury in HIV infected smokers, hastening the development of COPD. The mechanisms will be directly tested using blood and bronchial alveolar lavage (BAL) cells from smokers and nonsmokers with and without HIV infection.
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Immunosuppressive Effects of Smoking and HIV-1 on the Development of Lung Disease.|
- The change in immunoregulatory markers: PD-1 expression and interleukin (IL)-10 production by alveolar macrophages (AMs) from baseline to week 24. [ Time Frame: Baseline, Week 24 ] [ Designated as safety issue: No ]Evaluate the immunoregulatory change between HIV positive (smokers/non-smokers) and HIV negative (smokers/non-smokers)
- PD-1 expression and IL-10 production by AMs at baseline [ Time Frame: Baseline ] [ Designated as safety issue: No ]Evaluate the association of PD-1 expression and IL-10 production by AMs after long-term antiretroviral therapy (ART) with abnormal lung function and a COPD phenotype between HIV positive (with and without COPD) and HIV negative with COPD.
Biospecimen Retention: Samples Without DNA
|Study Start Date:||March 2014|
|Estimated Study Completion Date:||July 2018|
|Estimated Primary Completion Date:||July 2017 (Final data collection date for primary outcome measure)|
HIV positive smokers
HIV positive non-smokers
HIV negative smokers
HIV negative non-smokers
HIV positive with COPD
HIV positive without COPD (non-COPD)
HIV negative with COPD
The first component of this study will be a longitudinal, prospective, 24 weeks study of the effects of HIV-1 infection on innate and acquired immunity in the lung (Cohort A). The second component of this study will be a cross-sectional, case-control study of lung function and immune dysregulation of HIV-1 infected persons on long-term ART (Cohort B).
Cohort A will consist of 120 subjects, stratified by HIV-1 and smoking status
Cohort B will consist of 90 subjects stratified by chronic obstructive pulmonary disease (COPD) and HIV-1 infection.
Please refer to this study by its ClinicalTrials.gov identifier: NCT02058719
|Contact: Thomas B. Campbell, MDemail@example.com|
|Contact: Christine Griesmer, RNfirstname.lastname@example.org|
|United States, Colorado|
|University of Colorado Denver||Recruiting|
|Aurora, Colorado, United States, 80045|
|Contact: Thomas B. Campbell, MD 303-724-4929 email@example.com|
|Principal Investigator: Thomas B. Campbell, MD|
|Principal Investigator: Andrew Fontenot, MD|
|Principal Investigator:||Thomas B. Campbell, MD||University of Colorado, Denver|