NCT Number: NCT05227547
To evaluate the regenerative capacities of mesenchymal cells composing the microenvironment of alveolar type 2 cells in a population of patients, undergoing thoracic surgery for suspected cancer, who are smokers with and without COPD compared to non-smokers patients
Interested in participating?
Request Info18 year and older
All sexes
Interventional
Not applicable
Rousseau-Bussac, Créteil, France
Chronic obstructive pulmonary diseases (COPD) have a major public health impact, as evidenced by the 250 million patients affected by these diseases and the 50% 5-year mortality for severe stages of chronic obstructive pulmonary disease (COPD). One pathophysiological mechanism of COPD and emphysema is a depletion of alveolar progenitor cells inducing a loss of alveolar-reparation capacities after an aggression. The genesis of these alterations and the mechanisms involved remain unknown. Alveolar type 2 cells (AT2) are the alveolar epithelial progenitor cells. AT2 proliferate and differentiate into alveolar type 1 cells (AT1) which form the alveolar-capillary barrier, along with endothelial cells, through which respiratory gas exchanges take place. The proliferation and differentiation of AT2 into AT1 are under the control of mesenchymal cells and endothelial cells located in close proximity. Together these cells form the alveolar stem cell niche. The characteristics and interactions of the different cell populations have been well described during lung growth, in the normal adult lung or during pulmonary fibrosis; however, participants are poorly described during smoking exposure and chronic obstructive diseases.
Healthy volunteers accepted: No
Only the study team can determine whether someone qualifies for participation.
Inclusion criteria
Exclusion criteria
Patients undergoing thoracic resection surgery (pneumonectomy, lobectomy, segmentectomy) for cancer or suspected cancer, including smokers (active or ex-smokers) and non-smokers, with COPD and without COPD, and non-smoking patients.
Time frame: through study completion, an average of 3 years
Comparison of the number of alveolar organoids formed 21 days after culture of fibroblasts with alveolar type II cells between smokers with and without COPD and non-smoking patients
Time frame: through study completion, an average of 3 years
Evaluated by their doubling time, number of cells collected compared to the number of cells seeded
Time frame: through study completion, an average of 3 years
By immunofluorescence marking: number of alpha-smooth muscle actin (alpha-SMA) + cells compared to total cells
Time frame: through study completion, an average of 3 years
Evaluated in Boyden chamber
Time frame: through study completion, an average of 3 years
Evaluated by Ribonucleic acid (RNA) sequencing of fibroblasts
Time frame: through study completion, an average of 3 years
Evaluated byRibonucleic acid (RNA) sequencing of endothelial cells
Time frame: through study completion, an average of 3 years
Evaluated by Luminex Assay
Time frame: through study completion, an average of 3 years
By studying the migration and invasion of tumor cells
Time frame: through study completion, an average of 3 years
Cell types composing the lung stem cell microenvironment measured by single cell analysis
Time frame: At inclusion, every year, up to 5 years after surgery
Change of lung density assessed by computed tomography scan
Time frame: At inclusion, every year, up to 5 years after surgery
Assessed by computed tomography scan :
[centro-lobular or pan-lobular, para-septal]
Time frame: through study completion, an average of 3 years
Searched according to the results obtained during cell cultures (immunohistochemistry, immunofluorescence)
Time frame: through study completion, an average of 3 years
Evaluated in laboratory by metagenomic analysis of 16s Ribonucleic acid (RNA) of bacteria for cluster analysis that correlate with lung injury and could be prognostic markers
Time frame: through study completion, an average of 3 years
Evaluated in laboratory by metagenomic analysis of 16s Ribonucleic acid (RNA) of bacteria for cluster analysis that correlate with lung injury and could be prognostic markers
Time frame: through study completion, an average of 3 years
Determine the relationship between respiratory disease phenotype and exercise impact by measurement of Forced expiratory volume at one second (FEV1)
Time frame: through study completion, an average of 3 years
Determine the relationship between respiratory disease phenotype and exercise impact by measurement of Forced Vital Capacity (FVC )
Time frame: through study completion, an average of 3 years
Determine the relationship between respiratory disease phenotype and exercise impact by measurement of pulmonary diffusion capacity of CO (DLCO)
Time frame: through study completion, an average of 3 years
Determine the relationship between respiratory disease phenotype and exercise impact by measurement of CO transfer coefficient (KCO)
Contact information is provided by the study sponsor or research team.
Centre Hospitalier Intercommunal Creteil
Other
Acronym: CoStemCells
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