<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT03010592</url>
  </required_header>
  <id_info>
    <org_study_id>217587</org_study_id>
    <nct_id>NCT03010592</nct_id>
  </id_info>
  <brief_title>Studying the Airway Microenvironment in Patients Undergoing Surgical and Bronchoscopic Interventions for COPD</brief_title>
  <acronym>COPD-ENVIRON</acronym>
  <official_title>Studying the Airway Microenvironment in Patients Undergoing Surgical and Bronchoscopic Interventions for COPD</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Royal Brompton &amp; Harefield NHS Foundation Trust</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Royal Brompton &amp; Harefield NHS Foundation Trust</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      Studying the airway microenvironment in patients undergoing surgical and bronchoscopic&#xD;
      interventions for COPD&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Chronic obstructive pulmonary disease (COPD) is an umbrella term encompassing two entities&#xD;
      causing progressive and ultimately disabling breathlessness. Emphysema is a process&#xD;
      destructive of the airspaces distal to the terminal bronchioles, with loss of gas exchange&#xD;
      tissue, of elastic recoil and of circumferential tethering of the small airways leading to&#xD;
      their collapse on forced expiration. Chronic bronchitis is a disorder of the bronchi causing&#xD;
      excess production and impaired mobilisation of mucus. Increased parasympathetic tone and&#xD;
      progressive remodelling of airways impairs response to bronchodilators. Static and dynamic&#xD;
      hyperinflation ensue - a persistently expanded chest and flattened diaphragms despite&#xD;
      increasing use of accessory respiratory muscles - resulting in a disadvantaged respiratory&#xD;
      pump.&#xD;
&#xD;
      Patients with severe emphysema and hyperinflation benefit from lung volume reduction&#xD;
      techniques designed to reduce gas trapping and to improve airflow, chest wall and lung&#xD;
      mechanics. The best evidence exists for lung volume reduction surgery (LVRS), which however&#xD;
      is not without risk and there is increasing interest in the development of bronchoscopic lung&#xD;
      volume reduction (BLVR) techniques including emplacement of endobronchial valves and coils&#xD;
      and targeted lung denervation (TLD), which have all been shown to improve lung function,&#xD;
      exercise capacity, and quality of life.&#xD;
&#xD;
      Endobronchial cryotherapy is a novel investigational treatment in patients with chronic&#xD;
      bronchitis. Porcine models have shown ablation of abnormal metaplastic goblet cells and&#xD;
      regeneration of healthy ciliated epithelium and submucosa within 48 hours with complete&#xD;
      healing by 60 days following treatment. A pilot study evaluated 11 patients undergoing a&#xD;
      lobectomy or pneumonectomy for presumed lung cancer. Metered sprays, one to each of two&#xD;
      separate locations, were administered 2 weeks prior to surgery, at least 2cm distal to the&#xD;
      proposed resection margin (first segmental and lobular bronchi). No adverse events were&#xD;
      reported. Histology of the 8 submitted specimens demonstrated localised cryothermic effect&#xD;
      extending to but not beyond the submucosa, and minimal inflammation.&#xD;
&#xD;
      Chronic airway infiltration by neutrophils, macrophages, and Th-1 predominant lymphocytes&#xD;
      driven by increased expression of inflammatory proteins, cytokines and chemokines, is&#xD;
      intensified during exacerbations. It is generally accepted that acute exacerbations&#xD;
      accelerate the decline in lung function in COPD. Recent studies have suggested a role for&#xD;
      microvesicles (MVs) in the pathogenesis of COPD, driving exacerbations. MVs are fragments of&#xD;
      cell membrane ranging from 0.1 to 1µm in diameter shed by almost all eukaryotic cells. They&#xD;
      are recognised to be key mediators of intercellular communication, transporting a variety of&#xD;
      molecular cargo including proteins and nucleic acids to distant cells, and have been&#xD;
      implicated in various inflammatory diseases including COPD. The majority of studies have&#xD;
      looked at circulating endothelial-derived MVs, which are elevated in patients with COPD, are&#xD;
      significantly higher during an exacerbation, and are predictive of rapid forced expiratory&#xD;
      volume in 1 second (FEV1) decline. However, there is a paucity of data on epithelial-derived&#xD;
      MVs within the lung. We know from acute lung injury models that alveolar macrophage-derived&#xD;
      microvesicles, which carry biologically active tumour necrosis factor, are rapidly released&#xD;
      during the early phase and may play a role in initiating the disease process.&#xD;
&#xD;
      Bronchoalveolar lavage and brushings are established techniques to obtain material for&#xD;
      respectively, measurement of inflammatory proteins and microvesicles, and for cytology and&#xD;
      messenger ribonucleic acid (mRNA) analysis. A novel technique sampling the mucosal lining&#xD;
      fluid using a synthetic absorptive matrix ('bronchosorption') has been shown to have greater&#xD;
      sensitivity to standard bronchoalveolar lavage (BAL), eliminating the disadvantage of&#xD;
      dilution.&#xD;
&#xD;
      A combination of all three techniques to directly harvest lower airway samples at multiples&#xD;
      sites of pulmonary inflammation would allow comparison of proteomic, transcriptomic, and&#xD;
      histology data from the endobronchial environment before and after intervention. This would&#xD;
      be the first study evaluating the lung microenvironment in this context, which may identify&#xD;
      predictive biomarkers of response to intervention and future exacerbation risk.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Recruiting</last_known_status>
  <start_date type="Actual">February 6, 2017</start_date>
  <completion_date type="Anticipated">January 1, 2023</completion_date>
  <primary_completion_date type="Anticipated">January 1, 2023</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Other</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>Change from baseline in airway cytokine levels at 3 months follow-up</measure>
    <time_frame>Baseline versus 3 months follow-up</time_frame>
    <description>Change in airway cytokine levels measured using a multiplex assay, 3 months following interventional treatment</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Association between baseline cytokine levels and future exacerbation frequency at 3 months follow-up</measure>
    <time_frame>Baseline versus 3 months follow-up</time_frame>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Association between baseline cytokine levels and future decline in lung function at 3 months follow-up</measure>
    <time_frame>Baseline versus 3 months follow-up</time_frame>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Association between baseline microvesicle levels and future exacerbation frequency at 3 months follow-up</measure>
    <time_frame>Baseline versus 3 months follow-up</time_frame>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Association between baseline microvesicle levels and future decline in lung function at 3 months follow-up</measure>
    <time_frame>Baseline versus 3 months follow-up</time_frame>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Change from baseline in airway microvesicle levels at 3 months follow-up</measure>
    <time_frame>Baseline versus 3 months follow-up</time_frame>
    <description>Change in airway microvesicle levels measured using flow cytometry, 3 months following interventional treatment</description>
  </secondary_outcome>
  <enrollment type="Anticipated">80</enrollment>
  <condition>Chronic Obstructive Pulmonary Disease</condition>
  <condition>Emphysema</condition>
  <condition>Chronic Bronchitis</condition>
  <eligibility>
    <study_pop>
      <textblock>
        Patients with severe COPD who are scheduled to undergo surgical or bronchoscopic lung&#xD;
        intervention (n=80)&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Non-Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Scheduled for lung volume reduction treatment or endobronchial cryotherapy for the&#xD;
             management of severe COPD.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Unwilling or unable to sign the informed consent form&#xD;
&#xD;
          -  Patients with known Category 3 Organisms as per the Advisory Committee on Dangerous&#xD;
             Pathogens (ACDP) for example, Tuberculosis or Human Immunodeficiency Virus.&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>40 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Pallav L Shah, MBBS MD FRCP</last_name>
    <role>Principal Investigator</role>
    <affiliation>Royal Brompton &amp; Harefields Hospital</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>Justin L Garner, MBBS MRCP</last_name>
    <phone>02073518029</phone>
    <email>J.Garner@rbht.nhs.uk</email>
  </overall_contact>
  <location>
    <facility>
      <name>Chelsea &amp; Westminster Hospital</name>
      <address>
        <city>London</city>
        <state>Chelsea</state>
        <zip>SW3 6NP</zip>
        <country>United Kingdom</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>Nadia Shabbir</last_name>
      <phone>02033156684</phone>
      <email>Nadia.Shabbir@chelwest.nhs.uk</email>
    </contact>
    <investigator>
      <last_name>Masao Takata, Professor</last_name>
      <role>Principal Investigator</role>
    </investigator>
    <investigator>
      <last_name>Suveer Singh, MBBS PhD</last_name>
      <role>Sub-Investigator</role>
    </investigator>
    <investigator>
      <last_name>Kieran O'Dea, PhD</last_name>
      <role>Sub-Investigator</role>
    </investigator>
    <investigator>
      <last_name>Michael R Wilson, PhD</last_name>
      <role>Sub-Investigator</role>
    </investigator>
    <investigator>
      <last_name>Sanooj Soni, MBBS MRCP</last_name>
      <role>Sub-Investigator</role>
    </investigator>
    <investigator>
      <last_name>Pallav L Shah, MBBS FRCP</last_name>
      <role>Principal Investigator</role>
    </investigator>
  </location>
  <location>
    <facility>
      <name>Royal Brompton &amp; Harefields Hospital</name>
      <address>
        <city>London</city>
        <state>Fulham</state>
        <zip>SW3 6NP</zip>
        <country>United Kingdom</country>
      </address>
    </facility>
    <status>Not yet recruiting</status>
    <contact>
      <last_name>Patrik Patrik Pettersson</last_name>
      <phone>02073528121</phone>
      <email>p.pettersson@rbht.nhs.uk</email>
    </contact>
    <investigator>
      <last_name>Pallav L Shah, MBBS MD FRCP</last_name>
      <role>Principal Investigator</role>
    </investigator>
    <investigator>
      <last_name>Samuel V Kemp, MBBS MD MRCP</last_name>
      <role>Sub-Investigator</role>
    </investigator>
    <investigator>
      <last_name>Justin Garner, MBBS MRCP</last_name>
      <role>Sub-Investigator</role>
    </investigator>
    <investigator>
      <last_name>Karthi Srikanthan, MBBS MRCP</last_name>
      <role>Sub-Investigator</role>
    </investigator>
  </location>
  <location_countries>
    <country>United Kingdom</country>
  </location_countries>
  <results_reference>
    <citation>Barnes PJ. Immunology of asthma and chronic obstructive pulmonary disease. Nat Rev Immunol. 2008 Mar;8(3):183-92. doi: 10.1038/nri2254. Epub 2008 Feb 15.</citation>
    <PMID>18274560</PMID>
  </results_reference>
  <results_reference>
    <citation>Donaldson GC, Seemungal TA, Bhowmik A, Wedzicha JA. Relationship between exacerbation frequency and lung function decline in chronic obstructive pulmonary disease. Thorax. 2002 Oct;57(10):847-52. doi: 10.1136/thorax.57.10.847. Erratum In: Thorax. 2008 Aug;63(8):753.</citation>
    <PMID>12324669</PMID>
  </results_reference>
  <results_reference>
    <citation>Takahashi T, Kobayashi S, Fujino N, Suzuki T, Ota C, He M, Yamada M, Suzuki S, Yanai M, Kurosawa S, Yamaya M, Kubo H. Increased circulating endothelial microparticles in COPD patients: a potential biomarker for COPD exacerbation susceptibility. Thorax. 2012 Dec;67(12):1067-74. doi: 10.1136/thoraxjnl-2011-201395. Epub 2012 Jul 27.</citation>
    <PMID>22843558</PMID>
  </results_reference>
  <results_reference>
    <citation>Eltom S, Dale N, Raemdonck KR, Stevenson CS, Snelgrove RJ, Sacitharan PK, Recchi C, Wavre-Shapton S, McAuley DF, O'Kane C, Belvisi MG, Birrell MA. Respiratory infections cause the release of extracellular vesicles: implications in exacerbation of asthma/COPD. PLoS One. 2014 Jun 27;9(6):e101087. doi: 10.1371/journal.pone.0101087. eCollection 2014.</citation>
    <PMID>24972036</PMID>
  </results_reference>
  <results_reference>
    <citation>Raposo G, Stoorvogel W. Extracellular vesicles: exosomes, microvesicles, and friends. J Cell Biol. 2013 Feb 18;200(4):373-83. doi: 10.1083/jcb.201211138.</citation>
    <PMID>23420871</PMID>
  </results_reference>
  <results_reference>
    <citation>Nieri D, Neri T, Petrini S, Vagaggini B, Paggiaro P, Celi A. Cell-derived microparticles and the lung. Eur Respir Rev. 2016 Sep;25(141):266-77. doi: 10.1183/16000617.0009-2016.</citation>
    <PMID>27581826</PMID>
  </results_reference>
  <results_reference>
    <citation>Gordon C, Gudi K, Krause A, Sackrowitz R, Harvey BG, Strulovici-Barel Y, Mezey JG, Crystal RG. Circulating endothelial microparticles as a measure of early lung destruction in cigarette smokers. Am J Respir Crit Care Med. 2011 Jul 15;184(2):224-32. doi: 10.1164/rccm.201012-2061OC. Epub 2011 Mar 11.</citation>
    <PMID>21471087</PMID>
  </results_reference>
  <results_reference>
    <citation>Thomashow MA, Shimbo D, Parikh MA, Hoffman EA, Vogel-Claussen J, Hueper K, Fu J, Liu CY, Bluemke DA, Ventetuolo CE, Doyle MF, Barr RG. Endothelial microparticles in mild chronic obstructive pulmonary disease and emphysema. The Multi-Ethnic Study of Atherosclerosis Chronic Obstructive Pulmonary Disease study. Am J Respir Crit Care Med. 2013 Jul 1;188(1):60-8. doi: 10.1164/rccm.201209-1697OC.</citation>
    <PMID>23600492</PMID>
  </results_reference>
  <results_reference>
    <citation>Takahashi T, Kobayashi S, Fujino N, Suzuki T, Ota C, Tando Y, Yamada M, Yanai M, Yamaya M, Kurosawa S, Yamauchi M, Kubo H. Annual FEV1 changes and numbers of circulating endothelial microparticles in patients with COPD: a prospective study. BMJ Open. 2014 Mar 6;4(3):e004571. doi: 10.1136/bmjopen-2013-004571.</citation>
    <PMID>24604485</PMID>
  </results_reference>
  <results_reference>
    <citation>Soni S, Wilson MR, O'Dea KP, Yoshida M, Katbeh U, Woods SJ, Takata M. Alveolar macrophage-derived microvesicles mediate acute lung injury. Thorax. 2016 Nov;71(11):1020-1029. doi: 10.1136/thoraxjnl-2015-208032. Epub 2016 Jun 10.</citation>
    <PMID>27287089</PMID>
  </results_reference>
  <results_reference>
    <citation>Leaker BR, Nicholson GC, Ali FY, Daudi N, O'Connor BJ, Barnes PJ. Bronchoabsorption; a novel bronchoscopic technique to improve biomarker sampling of the airway. Respir Res. 2015 Sep 4;16(1):102. doi: 10.1186/s12931-015-0268-5.</citation>
    <PMID>26338015</PMID>
  </results_reference>
  <verification_date>September 2021</verification_date>
  <study_first_submitted>December 20, 2016</study_first_submitted>
  <study_first_submitted_qc>January 4, 2017</study_first_submitted_qc>
  <study_first_posted type="Estimate">January 5, 2017</study_first_posted>
  <last_update_submitted>September 14, 2021</last_update_submitted>
  <last_update_submitted_qc>September 14, 2021</last_update_submitted_qc>
  <last_update_posted type="Actual">September 16, 2021</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <keyword>Lung volume reduction treatment</keyword>
  <keyword>Endobronchial cryotherapy</keyword>
  <keyword>Microvesicles</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Bronchitis</mesh_term>
    <mesh_term>Bronchitis, Chronic</mesh_term>
    <mesh_term>Lung Diseases, Obstructive</mesh_term>
    <mesh_term>Pulmonary Disease, Chronic Obstructive</mesh_term>
    <mesh_term>Emphysema</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT03010592
org study id: 217587
nct id: NCT03010592
lead sponsor: 
has dmc: No
Studying the airway microenvironment in patients undergoing surgical and bronchoscopic
      interventions for COPD
Chronic obstructive pulmonary disease (COPD) is an umbrella term encompassing two entities
      causing progressive and ultimately disabling breathlessness. Emphysema is a process
      destructive of the airspaces distal to the terminal bronchioles, with loss of gas exchange
      tissue, of elastic recoil and of circumferential tethering of the small airways leading to
      their collapse on forced expiration. Chronic bronchitis is a disorder of the bronchi causing
      excess production and impaired mobilisation of mucus. Increased parasympathetic tone and
      progressive remodelling of airways impairs response to bronchodilators. Static and dynamic
      hyperinflation ensue - a persistently expanded chest and flattened diaphragms despite
      increasing use of accessory respiratory muscles - resulting in a disadvantaged respiratory
      pump.

      Patients with severe emphysema and hyperinflation benefit from lung volume reduction
      techniques designed to reduce gas trapping and to improve airflow, chest wall and lung
      mechanics. The best evidence exists for lung volume reduction surgery (LVRS), which however
      is not without risk and there is increasing interest in the development of bronchoscopic lung
      volume reduction (BLVR) techniques including emplacement of endobronchial valves and coils
      and targeted lung denervation (TLD), which have all been shown to improve lung function,
      exercise capacity, and quality of life.

      Endobronchial cryotherapy is a novel investigational treatment in patients with chronic
      bronchitis. Porcine models have shown ablation of abnormal metaplastic goblet cells and
      regeneration of healthy ciliated epithelium and submucosa within 48 hours with complete
      healing by 60 days following treatment. A pilot study evaluated 11 patients undergoing a
      lobectomy or pneumonectomy for presumed lung cancer. Metered sprays, one to each of two
      separate locations, were administered 2 weeks prior to surgery, at least 2cm distal to the
      proposed resection margin (first segmental and lobular bronchi). No adverse events were
      reported. Histology of the 8 submitted specimens demonstrated localised cryothermic effect
      extending to but not beyond the submucosa, and minimal inflammation.

      Chronic airway infiltration by neutrophils, macrophages, and Th-1 predominant lymphocytes
      driven by increased expression of inflammatory proteins, cytokines and chemokines, is
      intensified during exacerbations. It is generally accepted that acute exacerbations
      accelerate the decline in lung function in COPD. Recent studies have suggested a role for
      microvesicles (MVs) in the pathogenesis of COPD, driving exacerbations. MVs are fragments of
      cell membrane ranging from 0.1 to 1µm in diameter shed by almost all eukaryotic cells. They
      are recognised to be key mediators of intercellular communication, transporting a variety of
      molecular cargo including proteins and nucleic acids to distant cells, and have been
      implicated in various inflammatory diseases including COPD. The majority of studies have
      looked at circulating endothelial-derived MVs, which are elevated in patients with COPD, are
      significantly higher during an exacerbation, and are predictive of rapid forced expiratory
      volume in 1 second (FEV1) decline. However, there is a paucity of data on epithelial-derived
      MVs within the lung. We know from acute lung injury models that alveolar macrophage-derived
      microvesicles, which carry biologically active tumour necrosis factor, are rapidly released
      during the early phase and may play a role in initiating the disease process.

      Bronchoalveolar lavage and brushings are established techniques to obtain material for
      respectively, measurement of inflammatory proteins and microvesicles, and for cytology and
      messenger ribonucleic acid (mRNA) analysis. A novel technique sampling the mucosal lining
      fluid using a synthetic absorptive matrix ('bronchosorption') has been shown to have greater
      sensitivity to standard bronchoalveolar lavage (BAL), eliminating the disadvantage of
      dilution.

      A combination of all three techniques to directly harvest lower airway samples at multiples
      sites of pulmonary inflammation would allow comparison of proteomic, transcriptomic, and
      histology data from the endobronchial environment before and after intervention. This would
      be the first study evaluating the lung microenvironment in this context, which may identify
      predictive biomarkers of response to intervention and future exacerbation risk.
observational model: Other
time perspective: Prospective
measure: Change from baseline in airway cytokine levels at 3 months follow-up
time frame: Baseline versus 3 months follow-up
description: Change in airway cytokine levels measured using a multiplex assay, 3 months following interventional treatment
measure: Association between baseline cytokine levels and future exacerbation frequency at 3 months follow-up
time frame: Baseline versus 3 months follow-up
measure: Association between baseline cytokine levels and future decline in lung function at 3 months follow-up
time frame: Baseline versus 3 months follow-up
measure: Association between baseline microvesicle levels and future exacerbation frequency at 3 months follow-up
time frame: Baseline versus 3 months follow-up
measure: Association between baseline microvesicle levels and future decline in lung function at 3 months follow-up
time frame: Baseline versus 3 months follow-up
measure: Change from baseline in airway microvesicle levels at 3 months follow-up
time frame: Baseline versus 3 months follow-up
description: Change in airway microvesicle levels measured using flow cytometry, 3 months following interventional treatment
study pop: 
sampling method: Non-Probability Sample
criteria: 
gender: All
minimum age: 40 Years
maximum age: N/A
healthy volunteers: No
last name: Pallav L Shah, MBBS MD FRCP
role: Principal Investigator
affiliation: Royal Brompton & Harefields Hospital
last name: Justin L Garner, MBBS MRCP
phone: 02073518029
email: J.Garner@rbht.nhs.uk
facility: 
status: Recruiting
contact: 
investigator: 
investigator: 
investigator: 
investigator: 
investigator: 
investigator: 
facility: 
status: Not yet recruiting
contact: 
investigator: 
investigator: 
investigator: 
investigator: 
country: United Kingdom
citation: Barnes PJ. Immunology of asthma and chronic obstructive pulmonary disease. Nat Rev Immunol. 2008 Mar;8(3):183-92. doi: 10.1038/nri2254. Epub 2008 Feb 15.
PMID: 18274560
citation: Donaldson GC, Seemungal TA, Bhowmik A, Wedzicha JA. Relationship between exacerbation frequency and lung function decline in chronic obstructive pulmonary disease. Thorax. 2002 Oct;57(10):847-52. doi: 10.1136/thorax.57.10.847. Erratum In: Thorax. 2008 Aug;63(8):753.
PMID: 12324669
citation: Takahashi T, Kobayashi S, Fujino N, Suzuki T, Ota C, He M, Yamada M, Suzuki S, Yanai M, Kurosawa S, Yamaya M, Kubo H. Increased circulating endothelial microparticles in COPD patients: a potential biomarker for COPD exacerbation susceptibility. Thorax. 2012 Dec;67(12):1067-74. doi: 10.1136/thoraxjnl-2011-201395. Epub 2012 Jul 27.
PMID: 22843558
citation: Eltom S, Dale N, Raemdonck KR, Stevenson CS, Snelgrove RJ, Sacitharan PK, Recchi C, Wavre-Shapton S, McAuley DF, O'Kane C, Belvisi MG, Birrell MA. Respiratory infections cause the release of extracellular vesicles: implications in exacerbation of asthma/COPD. PLoS One. 2014 Jun 27;9(6):e101087. doi: 10.1371/journal.pone.0101087. eCollection 2014.
PMID: 24972036
citation: Raposo G, Stoorvogel W. Extracellular vesicles: exosomes, microvesicles, and friends. J Cell Biol. 2013 Feb 18;200(4):373-83. doi: 10.1083/jcb.201211138.
PMID: 23420871
citation: Nieri D, Neri T, Petrini S, Vagaggini B, Paggiaro P, Celi A. Cell-derived microparticles and the lung. Eur Respir Rev. 2016 Sep;25(141):266-77. doi: 10.1183/16000617.0009-2016.
PMID: 27581826
citation: Gordon C, Gudi K, Krause A, Sackrowitz R, Harvey BG, Strulovici-Barel Y, Mezey JG, Crystal RG. Circulating endothelial microparticles as a measure of early lung destruction in cigarette smokers. Am J Respir Crit Care Med. 2011 Jul 15;184(2):224-32. doi: 10.1164/rccm.201012-2061OC. Epub 2011 Mar 11.
PMID: 21471087
citation: Thomashow MA, Shimbo D, Parikh MA, Hoffman EA, Vogel-Claussen J, Hueper K, Fu J, Liu CY, Bluemke DA, Ventetuolo CE, Doyle MF, Barr RG. Endothelial microparticles in mild chronic obstructive pulmonary disease and emphysema. The Multi-Ethnic Study of Atherosclerosis Chronic Obstructive Pulmonary Disease study. Am J Respir Crit Care Med. 2013 Jul 1;188(1):60-8. doi: 10.1164/rccm.201209-1697OC.
PMID: 23600492
citation: Takahashi T, Kobayashi S, Fujino N, Suzuki T, Ota C, Tando Y, Yamada M, Yanai M, Yamaya M, Kurosawa S, Yamauchi M, Kubo H. Annual FEV1 changes and numbers of circulating endothelial microparticles in patients with COPD: a prospective study. BMJ Open. 2014 Mar 6;4(3):e004571. doi: 10.1136/bmjopen-2013-004571.
PMID: 24604485
citation: Soni S, Wilson MR, O'Dea KP, Yoshida M, Katbeh U, Woods SJ, Takata M. Alveolar macrophage-derived microvesicles mediate acute lung injury. Thorax. 2016 Nov;71(11):1020-1029. doi: 10.1136/thoraxjnl-2015-208032. Epub 2016 Jun 10.
PMID: 27287089
citation: Leaker BR, Nicholson GC, Ali FY, Daudi N, O'Connor BJ, Barnes PJ. Bronchoabsorption; a novel bronchoscopic technique to improve biomarker sampling of the airway. Respir Res. 2015 Sep 4;16(1):102. doi: 10.1186/s12931-015-0268-5.
PMID: 26338015
responsible party type: Sponsor
mesh term: Bronchitis
mesh term: Bronchitis, Chronic
mesh term: Lung Diseases, Obstructive
mesh term: Pulmonary Disease, Chronic Obstructive
mesh term: Emphysema
sharing ipd: No