COPD and Lung CancerNCT06483490
Environmental Pollutants in COPD and Lung Cancer
An observational study of COPD and Lung Cancer, run by University of Campania Luigi Vanvitelli at 1 site in Italy.
Trial summary
Epidemiological studies describe a statistically significant correlation between hospitalization rate and exposure to environmental pollutants such as atmospheric particulates (PM10 and PM2.5) and polycyclic aromatic hydrocarbons (PAH). Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- COPD and Lung Cancer
- What is being tested?
- This is a cross-sectional, non pharmacological study
- How many people
- 200 participants
- Where
- 1 siteItaly
- Study dates
- 1 May 2023to 1 May 2026
- Phase
- Observational
- 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 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Patients belong to UOC Interventional Pulmonology- Hospital Cardarelli and subjected to bronchoscopy, BAL and routine blood sampling following the clinical routine. All participants must sign the informed consent for participation in the study. All analyses to be carried out in this study will not require more human samples than is required by normal clinical practice. The excess amount of biological samples will be destroyed.
Who may be able to join
- All patients of both sexes and over the age of 18 years
- Clinical diagnosis of suspected lung cancer
Who cannot join
- Patients with infectious diseases,
- Patients with interstitiopathy
- Patients with autoimmune diseases
- Patients with cancers not covered by the inclusion criteria
- subjects on glucocorticoid therapy
- subjects who cannot undergo bronchial biopsy
- subjects who will not sign informed consent.
Trial locations and contacts
1 site in 1 country.
Italy1 site, 1 recruiting
- Recruiting
Cardarelli Hospital
Naples, 80131
Giuseppe Failla, MD, +390817473391, giuseppe.failla@aocardarelli.it
About this study
Official title: Mitochondrial Dysfunction and Immune Checkpoints in Chronic Obstructive Pulmonary Disease (COPD) and Lung Cancer: the Role of Environmental Pollutants
Epidemiological studies describe a statistically significant correlation between hospitalization rate and exposure to environmental pollutants such as atmospheric particulates (PM10 and PM2.5) and polycyclic aromatic hydrocarbons (PAH). Indeed, they induced the release of inflammation mediators and oxidative stress, involved in remodeling and destruction of the alveolar parenchyma, in turn associated with the respiratory disease onset and progression such as asthma, COPD, pulmonary fibrosis and lung cancer. Interestingly, oxidative stress associated with environmental pollutants could also induce DNA damage by affecting the stability of G-quadruplex (G4) sequences. Given the role of G4 in physiological and pathological processes and their presence in mitochondrial DNA, telomeres and proto-oncogene promoters, it is interesting to investigate the potential involvement in cellular mechanisms of response to oxidative stress associated with pollutants. Moreover, it is known that pollutant-induced oxidative stress has the ability to alter mitochondrial integrity, leading to mitochondrial dysfunction. The mitochondria involvement in the innate and adaptive immune response regulation corroborates the role of pollutants in respiratory diseases pathogenesis. Indeed, mitochondrial function and integrity are critical for both the effector and memory stages of differentiation of T cells which play a primary role in respiratory diseases. In this context, the PD-1/PD-L1 immune check-points are essential in promoting the immune system homeostasis. Currently, although the role of environmental pollutants, mitochondrial dysfunction and the PD-1/PD-L1 axis in the pathogenesis of many respiratory diseases is recognized, it is useful to further clarify the underlying molecular interconnections and the mechanisms by which pollutants could affect mitochondrial integrity and immune checkpoints.
Read the detailed description
Epidemiological studies describe a statistically significant correlation between hospitalization rate and exposure to environmental pollutants such as atmospheric particulates (PM10 and PM2.5). The harmfulness to human health depends on both the chemical composition and the particle size. Chronic exposure to particulate matter contributes to the risk of developing respiratory and cardiovascular diseases as well as may increase the risk of lung cancer. In fact, particulate matter is universally recognized as a Class 1 carcinogen. The fine particulates are harmful for human health by the ability to carry other pollutants such as polycyclic aromatic hydrocarbons (PAHs) to the lungs. Notably, the PAHs cause lung damage due to their ability to induce the release of inflammatory mediators and oxidative stress. These events result in remodeling and destruction of the alveolar parenchyma, both involved in respiratory disease onset and progression such as asthma, COPD, pulmonary fibrosis, and lung cancer. Therefore, the involvement of environmental pollutants in the predisposition and exacerbation of lung diseases, in the development of respiratory infections and in the process of carcinogenesis is evident. Moreover, in addition, oxidative stress associated with environmental pollutants could induce DNA damage. Recently, unconventional DNA structures have been identified, recognized as G-quadruplex (G4), which are particularly susceptible to oxidative stress. In fact, it is known that guanine-rich DNA sequences are more reactive with hydroxyl radicals than guanine residues scattered throughout the genome, and that oxidative damage (8-oxo-dg) formation at the G4 level reduces its thermal stability. Given the role of G4 in physiological and pathological processes and their presence in mitochondrial DNA, telomeres and proto-promoters oncogenes, it is interesting to investigate the potential involvement in cellular mechanisms of response to oxidative stress associated with pollutants. It is known that pollutant-induced oxidative stress has the ability to alter mitochondrial integrity, leading to mitochondrial dysfunction. Recent evidence points to innate immunity, apoptosis, and metabolism being largely regulated by mitochondrial activities. In turn, normal mitochondrial activity can be affected by inflammatory processes, infections, tobacco smoking and "environmental insults" and could respond to such stimuli through structural alterations and protein expression resulting in dysfunction. The mitochondria involvement in the innate and adaptive immune response regulation corroborates the role of pollutants in respiratory diseases pathogenesis. Indeed, mitochondrial function and integrity are critical for both the effector and memory stages of differentiation of T cells which play a primary role in respiratory diseases. In this context, the PD-1/PD-L1 immune check-points are essential in promoting the immune system homeostasis. Indeed, they take part in self-tolerance and consist of a series of ligand-receptor interactions involved in coordinating an effective immune response while limiting collateral damage to organs and tissues. The contribution of our research group in the study of the pathway PD-1/PD-L1 in the context of respiratory diseases was relevant, observing that this pathway is not only altered in lung cancer but also in chronic lung diseases such as COPD. Currently, although the role of environmental pollutants, mitochondrial dysfunction and the PD-1/PD-L1 axis in the pathogenesis of many respiratory diseases is recognized, it is useful to further clarify the underlying molecular interconnections and the mechanisms by which pollutants could affect mitochondrial integrity and immune checkpoints.
- Conditions
- COPD and Lung Cancer
- Being tested
- This is a cross-sectional, non pharmacological study
- Keywords
- COPD, Lung cancer, Mitochondrial dysfunction, immune checkpoints, Environmental pollution, cross-sectional, non-pharmacological, multicenter study
- Medical subject headings
- Pulmonary Disease, Chronic Obstructive, Lung Neoplasms, Mitochondrial Diseases
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
This is a cross-sectional, non pharmacological studyOther
Measurement of immune checkpoint levels, mitochondrial dysfunction, pollutant concentrations and G-quadruplex levels and their correlation in all enrolled subjects.
What is being measured
The primary outcome is the main question the study is designed to answer.
Immune checkpoints in COPD and lung cancer.
Measurement of immune checkpoint PD-L1, PD-1, e CTLA-4 levels in all enrolled subjects. The relative expression will be calculated by Real-time PCR using the comparative cycle threshold method (Ct) (2 - ΔΔCt).
Measured: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year
Mitochondrial activity in COPD and lung cancer.
Measurement of mitochondrial dysfunction markers in all enrolled subjects. ATP levels will be measured by means of the 'ATP bioluminescence assay kit' and the factors 'PTEN-induced kinase 1 (PINK)-Parkin-mediated pathway' (marker of mitophagy) and sirtuins (marker of senescence) by ELISA assay
Measured: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year.
Environmental pollutants in COPD and lung cancer.
Measurement of pollutant concentrations in all enrolled subjects. A fraction of BAL and peripheral blood will be used for the analysis of pollutants deposited on the cell surface and in the supernatant by means of gas chromatography (GC) coupled to mass spectrometry (MS).
Measured: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year.
G-quadruplex levels in all enrolled subjects.
Measurement of G-quadruplex levels in all enrolled subjects. The BG4 antibody will be used to evaluate the formation of G-quadruplex structures. Laser scanning confocal microscopy will be performed with a laser scanning confocal microscope with a 400X objective and the signal analysed with Fiji software.
Measured: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted3 Jul 2024
- Study start1 May 2023
- Primary completion1 May 2026 (estimated)
- Study completion1 May 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (5)Papers the sponsor has linked to this study.
- Other trials for COPD and Lung CancerStudies 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
- Observational
- Observational model
- Ecologic or community
- Time perspective
- Prospective
- Enrolment
- 200 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Campania Luigi Vanvitelli
- Sponsor type
- University, hospital or other
- Collaborators
- Cardarelli Hospital
- Responsible party
- Principal investigator, Prof. Bruno D'Agostino, PhD, MD, University of Campania Luigi Vanvitelli
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06483490
- Sponsor's protocol ID
- MITO2024
- Status last verified
- Jun 2024
- First submitted
- 19 Jun 2024
- Last updated
- 3 Jul 2024
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Wilkinson TMA. Immune checkpoints in chronic obstructive pulmonary disease. Eur Respir Rev. 2017 Jun 28;26(144):170045. doi: 10.1183/16000617.0045-2017. Print 2017 Jun 30.
PubMed 28659497Durham AL, Adcock IM. The relationship between COPD and lung cancer. Lung Cancer. 2015 Nov;90(2):121-7. doi: 10.1016/j.lungcan.2015.08.017. Epub 2015 Aug 29.
PubMed 26363803Wasen C, Erlandsson MC, Bossios A, Ekerljung L, Malmhall C, Toyra Silfversward S, Pullerits R, Lundback B, Bokarewa MI. Smoking Is Associated With Low Levels of Soluble PD-L1 in Rheumatoid Arthritis. Front Immunol. 2018 Jul 27;9:1677. doi: 10.3389/fimmu.2018.01677. eCollection 2018.
PubMed 30140263Prakash YS, Pabelick CM, Sieck GC. Mitochondrial Dysfunction in Airway Disease. Chest. 2017 Sep;152(3):618-626. doi: 10.1016/j.chest.2017.03.020. Epub 2017 Mar 21.
PubMed 28336486Sachdeva K, Do DC, Zhang Y, Hu X, Chen J, Gao P. Environmental Exposures and Asthma Development: Autophagy, Mitophagy, and Cellular Senescence. Front Immunol. 2019 Nov 29;10:2787. doi: 10.3389/fimmu.2019.02787. eCollection 2019.
PubMed 31849968
Study at a glance
From the registry record, last updated by the sponsor on 3 Jul 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Mitochondrial Dysfunction and Immune Checkpoints in Chronic Obstructive Pulmonary Disease (COPD) and Lung Cancer: the Role of Environmental Pollutants
- ClinicalTrials.gov ID
- NCT06483490
- Acronym / sponsor ID
- MITO2024
- Conditions
- COPD and Lung Cancer
- Keywords
- COPD, Lung cancer, Mitochondrial dysfunction, immune checkpoints, Environmental pollution, cross-sectional, non-pharmacological, multicenter study
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 200 participants (estimated)
- Lead sponsor
- University of Campania Luigi VanvitelliUniversity, hospital or other
- Collaborators
- Cardarelli Hospital
- Study start
- 1 May 2023 (actual)
- Primary completion
- 1 May 2026 (estimated)
- Study completion
- 1 May 2026 (estimated)
- First posted
- 3 Jul 2024 (actual)
- 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.
Epidemiological studies describe a statistically significant correlation between hospitalization rate and exposure to environmental pollutants such as atmospheric particulates (PM10 and PM2.5) and polycyclic aromatic hydrocarbons (PAH). Indeed, they induced the release of inflammation mediators and oxidative stress, involved in remodeling and destruction of the alveolar parenchyma, in turn associated with the respiratory disease onset and progression such as asthma, COPD, pulmonary fibrosis and lung cancer. Interestingly, oxidative stress associated with environmental pollutants could also induce DNA damage by affecting the stability of G-quadruplex (G4) sequences. Given the role of G4 in physiological and pathological processes and their presence in mitochondrial DNA, telomeres and proto-oncogene promoters, it is interesting to investigate the potential involvement in cellular mechanisms of response to oxidative stress associated with pollutants. Moreover, it is known that pollutant-induced oxidative stress has the ability to alter mitochondrial integrity, leading to mitochondrial dysfunction. The mitochondria involvement in the innate and adaptive immune response regulation corroborates the role of pollutants in respiratory diseases pathogenesis. Indeed, mitochondrial function and integrity are critical for both the effector and memory stages of differentiation of T cells which play a primary role in respiratory diseases. In this context, the PD-1/PD-L1 immune check-points are essential in promoting the immune system homeostasis. Currently, although the role of environmental pollutants, mitochondrial dysfunction and the PD-1/PD-L1 axis in the pathogenesis of many respiratory diseases is recognized, it is useful to further clarify the underlying molecular interconnections and the mechanisms by which pollutants could affect mitochondrial integrity and immune checkpoints.
Detailed description
Epidemiological studies describe a statistically significant correlation between hospitalization rate and exposure to environmental pollutants such as atmospheric particulates (PM10 and PM2.5). The harmfulness to human health depends on both the chemical composition and the particle size. Chronic exposure to particulate matter contributes to the risk of developing respiratory and cardiovascular diseases as well as may increase the risk of lung cancer. In fact, particulate matter is universally recognized as a Class 1 carcinogen. The fine particulates are harmful for human health by the ability to carry other pollutants such as polycyclic aromatic hydrocarbons (PAHs) to the lungs. Notably, the PAHs cause lung damage due to their ability to induce the release of inflammatory mediators and oxidative stress. These events result in remodeling and destruction of the alveolar parenchyma, both involved in respiratory disease onset and progression such as asthma, COPD, pulmonary fibrosis, and lung cancer. Therefore, the involvement of environmental pollutants in the predisposition and exacerbation of lung diseases, in the development of respiratory infections and in the process of carcinogenesis is evident. Moreover, in addition, oxidative stress associated with environmental pollutants could induce DNA damage. Recently, unconventional DNA structures have been identified, recognized as G-quadruplex (G4), which are particularly susceptible to oxidative stress. In fact, it is known that guanine-rich DNA sequences are more reactive with hydroxyl radicals than guanine residues scattered throughout the genome, and that oxidative damage (8-oxo-dg) formation at the G4 level reduces its thermal stability. Given the role of G4 in physiological and pathological processes and their presence in mitochondrial DNA, telomeres and proto-promoters oncogenes, it is interesting to investigate the potential involvement in cellular mechanisms of response to oxidative stress associated with pollutants. It is known that pollutant-induced oxidative stress has the ability to alter mitochondrial integrity, leading to mitochondrial dysfunction. Recent evidence points to innate immunity, apoptosis, and metabolism being largely regulated by mitochondrial activities. In turn, normal mitochondrial activity can be affected by inflammatory processes, infections, tobacco smoking and "environmental insults" and could respond to such stimuli through structural alterations and protein expression resulting in dysfunction. The mitochondria involvement in the innate and adaptive immune response regulation corroborates the role of pollutants in respiratory diseases pathogenesis. Indeed, mitochondrial function and integrity are critical for both the effector and memory stages of differentiation of T cells which play a primary role in respiratory diseases. In this context, the PD-1/PD-L1 immune check-points are essential in promoting the immune system homeostasis. Indeed, they take part in self-tolerance and consist of a series of ligand-receptor interactions involved in coordinating an effective immune response while limiting collateral damage to organs and tissues. The contribution of our research group in the study of the pathway PD-1/PD-L1 in the context of respiratory diseases was relevant, observing that this pathway is not only altered in lung cancer but also in chronic lung diseases such as COPD. Currently, although the role of environmental pollutants, mitochondrial dysfunction and the PD-1/PD-L1 axis in the pathogenesis of many respiratory diseases is recognized, it is useful to further clarify the underlying molecular interconnections and the mechanisms by which pollutants could affect mitochondrial integrity and immune checkpoints.
Study design
- Observational model
- Ecologic or community
- Time perspective
- Prospective
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients belong to UOC Interventional Pulmonology- Hospital Cardarelli and subjected to bronchoscopy, BAL and routine blood sampling following the clinical routine. All participants must sign the informed consent for participation in the study. All analyses to be carried out in this study will not require more human samples than is required by normal clinical practice. The excess amount of biological samples will be destroyed.
Key inclusion criteria (2 listed)
- All patients of both sexes and over the age of 18 years
- Clinical diagnosis of suspected lung cancer
Key exclusion criteria (7 listed)
- Patients with infectious diseases,
- Patients with interstitiopathy
- Patients with autoimmune diseases
- Patients with cancers not covered by the inclusion criteria
- subjects on glucocorticoid therapy
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 |
|---|---|---|
| This is a cross-sectional, non pharmacological studyMeasurement of immune checkpoint levels, mitochondrial dysfunction, pollutant concentrations and G-quadruplex levels and their correlation in all enrolled subjects. | Other | – |
Primary outcome
Immune checkpoints in COPD and lung cancer.
Time frame: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year
Measurement of immune checkpoint PD-L1, PD-1, e CTLA-4 levels in all enrolled subjects. The relative expression will be calculated by Real-time PCR using the comparative cycle threshold method (Ct) (2 - ΔΔCt).
Mitochondrial activity in COPD and lung cancer.
Time frame: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year.
Measurement of mitochondrial dysfunction markers in all enrolled subjects. ATP levels will be measured by means of the 'ATP bioluminescence assay kit' and the factors 'PTEN-induced kinase 1 (PINK)-Parkin-mediated pathway' (marker of mitophagy) and sirtuins (marker of senescence) by ELISA assay
Environmental pollutants in COPD and lung cancer.
Time frame: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year.
Measurement of pollutant concentrations in all enrolled subjects. A fraction of BAL and peripheral blood will be used for the analysis of pollutants deposited on the cell surface and in the supernatant by means of gas chromatography (GC) coupled to mass spectrometry (MS).
G-quadruplex levels in all enrolled subjects.
Time frame: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year.
Measurement of G-quadruplex levels in all enrolled subjects. The BG4 antibody will be used to evaluate the formation of G-quadruplex structures. Laser scanning confocal microscopy will be performed with a laser scanning confocal microscope with a 400X objective and the signal analysed with Fiji software.
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 Jul 2024.
- Background: PubMed 28659497Wilkinson TMA. Immune checkpoints in chronic obstructive pulmonary disease. Eur Respir Rev. 2017 Jun 28;26(144):170045. doi: 10.1183/16000617.0045-2017. Print 2017 Jun 30.
- Background: PubMed 26363803Durham AL, Adcock IM. The relationship between COPD and lung cancer. Lung Cancer. 2015 Nov;90(2):121-7. doi: 10.1016/j.lungcan.2015.08.017. Epub 2015 Aug 29.
- Background: PubMed 30140263Wasen C, Erlandsson MC, Bossios A, Ekerljung L, Malmhall C, Toyra Silfversward S, Pullerits R, Lundback B, Bokarewa MI. Smoking Is Associated With Low Levels of Soluble PD-L1 in Rheumatoid Arthritis. Front Immunol. 2018 Jul 27;9:1677. doi: 10.3389/fimmu.2018.01677. eCollection 2018.
- Background: PubMed 28336486Prakash YS, Pabelick CM, Sieck GC. Mitochondrial Dysfunction in Airway Disease. Chest. 2017 Sep;152(3):618-626. doi: 10.1016/j.chest.2017.03.020. Epub 2017 Mar 21.
- Background: PubMed 31849968Sachdeva K, Do DC, Zhang Y, Hu X, Chen J, Gao P. Environmental Exposures and Asthma Development: Autophagy, Mitophagy, and Cellular Senescence. Front Immunol. 2019 Nov 29;10:2787. doi: 10.3389/fimmu.2019.02787. eCollection 2019.
- 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.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of COPD and Lung Cancer, run by University of Campania Luigi Vanvitelli at 1 site in Italy.
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 2 inclusion and 7 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: status not confirmed, as of the sponsor's last update on 3 Jul 2024. 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 Italy. 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?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Bruno D'Agostino, MD, PhD (+393472601620, bruno.dagostino@unicampania.it), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Immune checkpoints in COPD and lung cancer. (time frame: The outcome will be measured once for each included patient after the enrollment through study completion, an average of 3 year). The study lists 4 primary outcomes in all. 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 NCT06483490, which also lists 5 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 Jul 2024.