Pulmonary Disease, Chronic ObstructiveNCT03034642
Modulation of Steroid Immunosuppression by Alveolar Efferocytosis
A study testing Bronchoscopy with bilateral bronchoalveolar lavages in people with Pulmonary Disease, Chronic Obstructive and Pneumonia, Bacterial, run by VA Ann Arbor Healthcare System at 1 site in United States.
Trial summary
The long-term goals of this study are (a) to understand the biological underpinnings for the increased incidence of community-acquired pneumonia in patients with chronic obstructive pulmonary disease (COPD) who are treated with inhaled corticosteroids; and (b) to develop novel therapies to treated this problem using… Read more about this study
- Who is it for?
- Ages 18 to 80 yearsHealthy volunteers can take part
- Conditions the study is for
- Pulmonary Disease, Chronic Obstructive, Pneumonia, Bacterial
- What is being tested?
- Bronchoscopy with bilateral bronchoalveolar lavages
- Type of treatment
- Surgery or procedure
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 60 participants
- Where
- 1 siteUnited States
- Study dates
- 1 Oct 2015to 30 Dec 2021
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 80 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Age 18-80 years, inclusive
- Males or females
- Never smoker (< 100 cigarettes in lifetime)
- OR
- Current smoker (>10 pack-years) with normal spirometry
- Able to perform satisfactory spirometry
Show all 20Show fewer
- Abe to give informed consent
- Able to complete questionnaires
- Age 18-80 years, inclusive
- Males or females
- Current smoker
- (>10 pack-years) \& (≥1/2 pack/day)
- OR
- Former smoker
- (>10 pack-years) \& (>6 months of non-smoking)
- Diagnosis of COPD by ATS/ERS1 criteria
- Able to perform satisfactory spirometry
- Able to give informed consent
- Able to complete questionnaires
- 1 ATS/ERS, American Thoracic Society/European Respiratory Society.
Who cannot join
- Unstable cardiovascular disease, including uncontrolled hypertension, CHF, angina
- Significant renal (creatinine >2.5) or hepatic dysfunction (Childs B or C)
- Mental incompetence/active psychiatric illness
- Prednisone or other immunosuppressive medications
- Participation in another interventional experimental protocol within 6 weeks
- Pregnancy
Show all 35Show fewer
- Use of antibiotics for any reason within 42 days
- Judged to be unsuitable for bronchoscopy by PI
- Resting SaO2<93%
- FEV1 < 70% predicted
- Respiratory infections within 42 days regardless of antibiotic use
- Diagnosed COPD or Asthma
- Use of inhaled corticosteroids
- Active pulmonary tuberculosis or other serious chronic respiratory infection
- Diffuse panbronchiolitis or Cystic fibrosis
- Clinically significant bronchiectasis
- History of thoracic radiation therapy for any cause
- Other inflammatory or fibrotic lung disease
- Unstable cardiovascular disease, including uncontrolled hypertension, CHF, angina
- Significant renal (creatinine >2.5) or hepatic dysfunction (Childs B or C)
- Mental incompetence/active psychiatric illness
- Prednisone or other immunosuppressive medications
- Participation in another interventional experimental protocol within 6 weeks
- Pregnancy
- Use of antibiotics for any reason within 42 days
- Judged to be unsuitable for bronchoscopy by PI
- Resting daytime SaO2<90% while breathing room air
- FEV1 < 50% predicted
- Respiratory infections within 42 days regardless of antibiotic use
- Use of inhaled corticosteroids
- Active pulmonary tuberculosis or other serious chronic respiratory infection
- Diffuse panbronchiolitis or Cystic fibrosis
- Clinically significant bronchiectasis
- History of thoracic radiation therapy for any cause
- Other inflammatory or fibrotic lung disease
Trial locations and contacts
1 site in 1 country.
United States1 site
VA Ann Arbor Healthcare System
Ann Arbor, Michigan, 48105
About this study
The long-term goals of this study are (a) to understand the biological underpinnings for the increased incidence of community-acquired pneumonia in patients with chronic obstructive pulmonary disease (COPD) who are treated with inhaled corticosteroids; and (b) to develop novel therapies to treated this problem using over-expression of micro-RNAs (miRNAs).
Read the detailed description
Treating chronic obstructive pulmonary disease (COPD) patients with inhaled glucocorticosteroids has been convincingly shown to increase their risk of pneumonia, but the responsible mechanisms are undefined. Work from this laboratory suggests a possible mechanism, related to the increased numbers of cells dying by apoptosis in the lungs in COPD, especially in emphysema. Uptake of apoptotic cells ("efferocytosis") suppresses the ability of alveolar macrophages (AM) to fight infections. By markedly increasing AM efferocytosis, glucocorticoids plus apoptotic cells cause greater immune defects than either stimulus alone. These defects include reductions in killing of Streptococcus pneumoniae by human AM and murine AM in vitro, and in clearance of viable pneumococci from lungs of mice. This effect is called glucocorticoid augmented efferocytosis (GCAE). MicroRNAs (miRNAs) are 19-25 nucleotide-long non-coding RNAs that coordinately target large numbers of genes and reduce their protein products. Preliminary data imply that defective AM function is caused by down-regulation of specific miRNAs by GCAE (but not by apoptotic cells alone or glucocorticosteroids alone). The long-term goal of this project is to develop novel inhalational treatments based on transient over-expression of these specifically decreased miRNAs, to reverse defective AM immune function when COPD patients taking inhaled glucocorticoids present with community-acquired pneumonia. This project will use both ex vivo investigation of AM from human volunteers (never-smokers; smokers with normal spirometry; and COPD subjects who are current or former smokers), and an established murine model of pneumococcal pneumonia. Its immediate goals are to: (a) confirm that GCAE increases pneumococcal pneumonia risk and severity, and in the process, validate a murine model for testing strategies to reverse those defects; (b) define GCAE-induced AM defects functionally and by whole-transcriptome analysis, identifying genes and miRNAs uniquely regulated by the GCAE x pneumococcus interaction; (c) validate and optimize miRNA-over-expression to reverse the adverse effects of GCAE on AM defensive functions. Successful completion of this project could lead to more precisely personalized therapies and better outcomes in COPD, currently the third leading cause of death in the USA
- Being tested
- Bronchoscopy with bilateral bronchoalveolar lavages
- Keywords
- Apoptosis, Bronchoscopy, Human, Mice, inbred strains, Macrophages, Alveolar, MicroRNAs, Streptococcus pneumoniae, Fluticasone
- Medical subject headings
- Pulmonary Disease, Chronic Obstructive, Pneumonia, Bacterial
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Bronchoscopy with bilateral bronchoalveolar lavagesProcedure or surgery
Bronchoscopy with bilateral bronchoalveolar lavages
| Study group | Role | What they receive |
|---|---|---|
| Healthy Participants | Experimental | Procedure/Surgery: Bronchoscopy with bilateral bronchoalveolar lavages.
Drugs: No test substances, only moderate conscious sedation using standard medications.
Devices: No test devices. Receives: Procedure: Bronchoscopy with bilateral bronchoalveolar lavages |
| COPD participants | Experimental | Procedure/Surgery: Bronchoscopy with bilateral bronchoalveolar lavages.
Drugs: No test substances, only moderate conscious sedation using standard medications.
Devices: No test devices. Receives: Procedure: Bronchoscopy with bilateral bronchoalveolar lavages |
What is being measured
The primary outcome is the main question the study is designed to answer.
Bactericidal activity of human alveolar macrophage against S. pneumoniae in vitro
Alveolar macrophages from volunteers will be be assayed for their ability to kill pneumococci in vitro following treatment with glucocorticoids, apoptotic cells or both. Participation of the subjects ends after bronchoscopy, and no clinical outcomes will be measured.
Measured: 24 hours
Secondary outcomes (1)
Mechanisms of human alveolar macrophage killing of S. pneumoniae in vitro
These same macrophages will also be assayed for production of mRNA and regulatory microRNAs (by RNA sequencing and quantitative real-time PCR and for cytokine and chemokine production.
Measured: 24 hours
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted27 Jan 2017 (estimated)
- Study start1 Oct 2015
- Primary completion20 Mar 2020
- Study completion30 Dec 2021
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (20)Papers the sponsor has linked to this study.
- Other trials for Pulmonary Disease, Chronic ObstructiveStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Model description
- This study will analyze both healthy subjects (never-smokers and current- or ex-smokers) in one arm, and also subjects with COPD (current- or ex-smokers).
- Masking
- None (open label)
- Enrolment
- 60 participants (actual)
Sponsor and investigators
- Lead sponsor
- VA Ann Arbor Healthcare System
- Sponsor type
- US federal agency
- Collaborators
- University of Michigan
- Responsible party
- Principal investigator, Jeffrey Curtis, VA Ann Arbor Healthcare System
- Investigators
- Jeffrey L. Curtis, M.D., Principal investigator, University of Michigan
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03034642
- Sponsor's protocol ID
- VAAAHS Curtis 0038
- Other IDs
- I01CX000911
- Status last verified
- Apr 2022
- First submitted
- 23 Jan 2017
- Last updated
- 3 May 2022
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
McCubbrey AL, Sonstein J, Ames TM, Freeman CM, Curtis JL. Glucocorticoids relieve collectin-driven suppression of apoptotic cell uptake in murine alveolar macrophages through downregulation of SIRPalpha. J Immunol. 2012 Jul 1;189(1):112-9. doi: 10.4049/jimmunol.1200984. Epub 2012 May 21.
PubMed 22615206Freeman CM, Martinez CH, Todt JC, Martinez FJ, Han MK, Thompson DL, McCloskey L, Curtis JL. Acute exacerbations of chronic obstructive pulmonary disease are associated with decreased CD4+ & CD8+ T cells and increased growth & differentiation factor-15 (GDF-15) in peripheral blood. Respir Res. 2015 Aug 5;16(1):94. doi: 10.1186/s12931-015-0251-1.
PubMed 26243260Adar SD, Huffnagle GB, Curtis JL. The respiratory microbiome: an underappreciated player in the human response to inhaled pollutants? Ann Epidemiol. 2016 May;26(5):355-9. doi: 10.1016/j.annepidem.2016.03.010. Epub 2016 Apr 7.
PubMed 27161078Huang YJ, Erb-Downward JR, Dickson RP, Curtis JL, Huffnagle GB, Han MK. Understanding the role of the microbiome in chronic obstructive pulmonary disease: principles, challenges, and future directions. Transl Res. 2017 Jan;179:71-83. doi: 10.1016/j.trsl.2016.06.007. Epub 2016 Jun 23.
PubMed 27392936Freeman CM, Curtis JL. Lung Dendritic Cells: Shaping Immune Responses throughout Chronic Obstructive Pulmonary Disease Progression. Am J Respir Cell Mol Biol. 2017 Feb;56(2):152-159. doi: 10.1165/rcmb.2016-0272TR.
PubMed 27767327Verhamme FM, Freeman CM, Brusselle GG, Bracke KR, Curtis JL. GDF-15 in Pulmonary and Critical Care Medicine. Am J Respir Cell Mol Biol. 2019 Jun;60(6):621-628. doi: 10.1165/rcmb.2018-0379TR.
PubMed 30633545Freeman CM, Curtis JL. It's Complicated: Lung Dendritic Cells in Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2020 Aug 15;202(4):479-481. doi: 10.1164/rccm.202004-0899ED. No abstract available.
PubMed 32286855Polverino F, Curtis JL. The ABCs of Granulomatous Lung Diseases: Age-associated B Cells. Am J Respir Crit Care Med. 2020 Oct 1;202(7):922-924. doi: 10.1164/rccm.202006-2261ED. No abstract available.
PubMed 32603192He Y, Wang H, Zheng J, Beiting DP, Masci AM, Yu H, Liu K, Wu J, Curtis JL, Smith B, Alekseyenko AV, Obeid JS. OHMI: the ontology of host-microbiome interactions. J Biomed Semantics. 2019 Dec 30;10(1):25. doi: 10.1186/s13326-019-0217-1.
PubMed 31888755Tighe RM, Redente EF, Yu YR, Herold S, Sperling AI, Curtis JL, Duggan R, Swaminathan S, Nakano H, Zacharias WJ, Janssen WJ, Freeman CM, Brinkman RR, Singer BD, Jakubzick CV, Misharin AV. Improving the Quality and Reproducibility of Flow Cytometry in the Lung. An Official American Thoracic Society Workshop Report. Am J Respir Cell Mol Biol. 2019 Aug;61(2):150-161. doi: 10.1165/rcmb.2019-0191ST.
PubMed 31368812Curtis JL. B Cells Caught in the Act: Class Switching to IgA in Lung Lymphoid Follicles in Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2019 Mar 1;199(5):548-550. doi: 10.1164/rccm.201810-1907ED. No abstract available.
PubMed 30352169Stolberg VR, McCubbrey AL, Freeman CM, Brown JP, Crudgington SW, Taitano SH, Saxton BL, Mancuso P, Curtis JL. Glucocorticoid-Augmented Efferocytosis Inhibits Pulmonary Pneumococcal Clearance in Mice by Reducing Alveolar Macrophage Bactericidal Function. J Immunol. 2015 Jul 1;195(1):174-84. doi: 10.4049/jimmunol.1402217. Epub 2015 May 18.
PubMed 25987742McCubbrey AL, Nelson JD, Stolberg VR, Blakely PK, McCloskey L, Janssen WJ, Freeman CM, Curtis JL. MicroRNA-34a Negatively Regulates Efferocytosis by Tissue Macrophages in Part via SIRT1. J Immunol. 2016 Feb 1;196(3):1366-75. doi: 10.4049/jimmunol.1401838. Epub 2015 Dec 30.
PubMed 26718338Dickson RP, Erb-Downward JR, Freeman CM, McCloskey L, Beck JM, Huffnagle GB, Curtis JL. Spatial Variation in the Healthy Human Lung Microbiome and the Adapted Island Model of Lung Biogeography. Ann Am Thorac Soc. 2015 Jun;12(6):821-30. doi: 10.1513/AnnalsATS.201501-029OC.
PubMed 25803243Dickson RP, Erb-Downward JR, Freeman CM, McCloskey L, Falkowski NR, Huffnagle GB, Curtis JL. Bacterial Topography of the Healthy Human Lower Respiratory Tract. mBio. 2017 Feb 14;8(1):e02287-16. doi: 10.1128/mBio.02287-16.
PubMed 28196961
Study at a glance
From the registry record, last updated by the sponsor on 3 May 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Modulation of Steroid Immunosuppression by Alveolar Efferocytosis
- ClinicalTrials.gov ID
- NCT03034642
- Acronym / sponsor ID
- VAAAHS Curtis 0038
- Keywords
- Apoptosis, Bronchoscopy, Human, Mice, inbred strains, Macrophages, Alveolar, MicroRNAs, Streptococcus pneumoniae, Fluticasone
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 60 participants (actual)
- Lead sponsor
- VA Ann Arbor Healthcare SystemUS federal agency
- Collaborators
- University of Michigan
- Study start
- 1 Oct 2015 (actual)
- Primary completion
- 20 Mar 2020 (actual)
- Study completion
- 30 Dec 2021 (actual)
- First posted
- 27 Jan 2017 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The long-term goals of this study are (a) to understand the biological underpinnings for the increased incidence of community-acquired pneumonia in patients with chronic obstructive pulmonary disease (COPD) who are treated with inhaled corticosteroids; and (b) to develop novel therapies to treated this problem using over-expression of micro-RNAs (miRNAs).
Detailed description
Treating chronic obstructive pulmonary disease (COPD) patients with inhaled glucocorticosteroids has been convincingly shown to increase their risk of pneumonia, but the responsible mechanisms are undefined. Work from this laboratory suggests a possible mechanism, related to the increased numbers of cells dying by apoptosis in the lungs in COPD, especially in emphysema. Uptake of apoptotic cells ("efferocytosis") suppresses the ability of alveolar macrophages (AM) to fight infections. By markedly increasing AM efferocytosis, glucocorticoids plus apoptotic cells cause greater immune defects than either stimulus alone. These defects include reductions in killing of Streptococcus pneumoniae by human AM and murine AM in vitro, and in clearance of viable pneumococci from lungs of mice. This effect is called glucocorticoid augmented efferocytosis (GCAE). MicroRNAs (miRNAs) are 19-25 nucleotide-long non-coding RNAs that coordinately target large numbers of genes and reduce their protein products. Preliminary data imply that defective AM function is caused by down-regulation of specific miRNAs by GCAE (but not by apoptotic cells alone or glucocorticosteroids alone). The long-term goal of this project is to develop novel inhalational treatments based on transient over-expression of these specifically decreased miRNAs, to reverse defective AM immune function when COPD patients taking inhaled glucocorticoids present with community-acquired pneumonia. This project will use both ex vivo investigation of AM from human volunteers (never-smokers; smokers with normal spirometry; and COPD subjects who are current or former smokers), and an established murine model of pneumococcal pneumonia. Its immediate goals are to: (a) confirm that GCAE increases pneumococcal pneumonia risk and severity, and in the process, validate a murine model for testing strategies to reverse those defects; (b) define GCAE-induced AM defects functionally and by whole-transcriptome analysis, identifying genes and miRNAs uniquely regulated by the GCAE x pneumococcus interaction; (c) validate and optimize miRNA-over-expression to reverse the adverse effects of GCAE on AM defensive functions. Successful completion of this project could lead to more precisely personalized therapies and better outcomes in COPD, currently the third leading cause of death in the USA
Study design
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- This study will analyze both healthy subjects (never-smokers and current- or ex-smokers) in one arm, and also subjects with COPD (current- or ex-smokers).
| Arm | Type | Receives |
|---|---|---|
| Healthy Participants | Experimental | Procedure: Bronchoscopy with bilateral bronchoalveolar lavagesProcedure/Surgery: Bronchoscopy with bilateral bronchoalveolar lavages. Drugs: No test substances, only moderate conscious sedation using standard medications. Devices: No test devices. |
| COPD participants | Experimental | Procedure: Bronchoscopy with bilateral bronchoalveolar lavagesProcedure/Surgery: Bronchoscopy with bilateral bronchoalveolar lavages. Drugs: No test substances, only moderate conscious sedation using standard medications. Devices: No test devices. |
Who may qualify
- Ages
- 18 to 80 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (20 listed)
- Age 18-80 years, inclusive
- Males or females
- Never smoker (< 100 cigarettes in lifetime)
- Current smoker (>10 pack-years) with normal spirometry
- Able to perform satisfactory spirometry
Key exclusion criteria (35 listed)
- Unstable cardiovascular disease, including uncontrolled hypertension, CHF, angina
- Significant renal (creatinine >2.5) or hepatic dysfunction (Childs B or C)
- Mental incompetence/active psychiatric illness
- Prednisone or other immunosuppressive medications
- Participation in another interventional experimental protocol within 6 weeks
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Bronchoscopy with bilateral bronchoalveolar lavagesBronchoscopy with bilateral bronchoalveolar lavages | Procedure or surgery | COPD participants, Healthy Participants |
Primary outcome
Bactericidal activity of human alveolar macrophage against S. pneumoniae in vitro
Time frame: 24 hours
Alveolar macrophages from volunteers will be be assayed for their ability to kill pneumococci in vitro following treatment with glucocorticoids, apoptotic cells or both. Participation of the subjects ends after bronchoscopy, and no clinical outcomes will be measured.
1 secondary outcome
Mechanisms of human alveolar macrophage killing of S. pneumoniae in vitro
Time frame: 24 hours
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 May 2022.
- Background: PubMed 22615206McCubbrey AL, Sonstein J, Ames TM, Freeman CM, Curtis JL. Glucocorticoids relieve collectin-driven suppression of apoptotic cell uptake in murine alveolar macrophages through downregulation of SIRPalpha. J Immunol. 2012 Jul 1;189(1):112-9. doi: 10.4049/jimmunol.1200984. Epub 2012 May 21.
- Background: PubMed 26243260Freeman CM, Martinez CH, Todt JC, Martinez FJ, Han MK, Thompson DL, McCloskey L, Curtis JL. Acute exacerbations of chronic obstructive pulmonary disease are associated with decreased CD4+ & CD8+ T cells and increased growth & differentiation factor-15 (GDF-15) in peripheral blood. Respir Res. 2015 Aug 5;16(1):94. doi: 10.1186/s12931-015-0251-1.
- Background: PubMed 27161078Adar SD, Huffnagle GB, Curtis JL. The respiratory microbiome: an underappreciated player in the human response to inhaled pollutants? Ann Epidemiol. 2016 May;26(5):355-9. doi: 10.1016/j.annepidem.2016.03.010. Epub 2016 Apr 7.
- Background: PubMed 27392936Huang YJ, Erb-Downward JR, Dickson RP, Curtis JL, Huffnagle GB, Han MK. Understanding the role of the microbiome in chronic obstructive pulmonary disease: principles, challenges, and future directions. Transl Res. 2017 Jan;179:71-83. doi: 10.1016/j.trsl.2016.06.007. Epub 2016 Jun 23.
- Background: PubMed 27767327Freeman CM, Curtis JL. Lung Dendritic Cells: Shaping Immune Responses throughout Chronic Obstructive Pulmonary Disease Progression. Am J Respir Cell Mol Biol. 2017 Feb;56(2):152-159. doi: 10.1165/rcmb.2016-0272TR.
- Background: PubMed 30633545Verhamme FM, Freeman CM, Brusselle GG, Bracke KR, Curtis JL. GDF-15 in Pulmonary and Critical Care Medicine. Am J Respir Cell Mol Biol. 2019 Jun;60(6):621-628. doi: 10.1165/rcmb.2018-0379TR.
- Background: PubMed 32286855Freeman CM, Curtis JL. It's Complicated: Lung Dendritic Cells in Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2020 Aug 15;202(4):479-481. doi: 10.1164/rccm.202004-0899ED. No abstract available.
- Background: PubMed 32603192Polverino F, Curtis JL. The ABCs of Granulomatous Lung Diseases: Age-associated B Cells. Am J Respir Crit Care Med. 2020 Oct 1;202(7):922-924. doi: 10.1164/rccm.202006-2261ED. No abstract available.
- Background: PubMed 31888755He Y, Wang H, Zheng J, Beiting DP, Masci AM, Yu H, Liu K, Wu J, Curtis JL, Smith B, Alekseyenko AV, Obeid JS. OHMI: the ontology of host-microbiome interactions. J Biomed Semantics. 2019 Dec 30;10(1):25. doi: 10.1186/s13326-019-0217-1.
- Background: PubMed 31368812Tighe RM, Redente EF, Yu YR, Herold S, Sperling AI, Curtis JL, Duggan R, Swaminathan S, Nakano H, Zacharias WJ, Janssen WJ, Freeman CM, Brinkman RR, Singer BD, Jakubzick CV, Misharin AV. Improving the Quality and Reproducibility of Flow Cytometry in the Lung. An Official American Thoracic Society Workshop Report. Am J Respir Cell Mol Biol. 2019 Aug;61(2):150-161. doi: 10.1165/rcmb.2019-0191ST.
- Background: PubMed 30352169Curtis JL. B Cells Caught in the Act: Class Switching to IgA in Lung Lymphoid Follicles in Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2019 Mar 1;199(5):548-550. doi: 10.1164/rccm.201810-1907ED. No abstract available.
- Results publication: PubMed 25987742Stolberg VR, McCubbrey AL, Freeman CM, Brown JP, Crudgington SW, Taitano SH, Saxton BL, Mancuso P, Curtis JL. Glucocorticoid-Augmented Efferocytosis Inhibits Pulmonary Pneumococcal Clearance in Mice by Reducing Alveolar Macrophage Bactericidal Function. J Immunol. 2015 Jul 1;195(1):174-84. doi: 10.4049/jimmunol.1402217. Epub 2015 May 18.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Jeffrey L. Curtis, M.D. principal investigator
University of Michigan
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Bronchoscopy with bilateral bronchoalveolar lavages in people with Pulmonary Disease, Chronic Obstructive and Pneumonia, Bacterial, run by VA Ann Arbor Healthcare System at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 20 inclusion and 35 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 3 May 2022. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Bactericidal activity of human alveolar macrophage against S. pneumoniae in vitro (time frame: 24 hours). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03034642, which also lists 20 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 3 May 2022.