Not provided
| ID | Type | Description | Link |
|---|---|---|---|
| 2013-14 | Other Identifier | AP HM |
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Asthma and COPD are characterized by an accelerated decline in lung function associated with incompletely reversible airflow obstruction. This could be the result of lung structural changes and inflammation. Tissue repairing mechanisms may result in a restitution ad integrum of bronchial epithelium. But in most cases, especially in COPD and severe asthma, the "remodeling" is characterized by mucus cells hyperplasia, overproduction of mucus, and physicochemical, biological and immunological changes. Clinically, this mucus overproduction is reported by patients as the clinical symptom called "chronic bronchitis". Generally, it develops at a bronchiolar level where it is responsible for the progression of these diseases. There is a paradox, because the intrinsic properties of mucus seem rather beneficial so fighting against it may not be really wise at long-term. Especially its defensive effect against microbial agents which remains poorly explained. Currently, no treatment aims to reduce the production of mucus and mechanisms leading to such an overproduction are poorly understood in severe asthma and COPD. The identification of new targets to treat this overproduction of mucus in COPD is therefore of major interest.
In view of current knowledge, inflammatory mediators and signal transduction leading to increased mucin production and increased number of goblet cells are probably IL-9, IL-13, IL -1ß and TNF-α involving calcium-sensitive chloride channels. Intracellular signaling pathways seem to be based on STAT-6, FOXA2, SPDEF, EGFR and / or COX-2
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
| Label | Type | Description | Intervention Names |
|---|---|---|---|
| smoking COPD | Experimental |
| |
| smoking without COPD | Experimental |
| |
| No Smoking Control | Other |
| |
| severe asthma | Experimental |
|
| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| bronchial biopsies | Procedure |
| ||
| Measure | Description | Time Frame |
|---|---|---|
| measure the impact of cigarette smoke on the formation and composition of mucus produced by the bronchial epithelium | (physicochemical properties, protein composition and potentially beneficial role in innate immunity) | 4 years |
| Measure | Description | Time Frame |
|---|---|---|
| measure the concentration of intracellular calcium | induced by cigarette smoke measured by confocal microscopy using a fluorochrome (Fura-2) | 4 years |
Not provided
Inclusion Criteria:
Exclusion Criteria:
Not provided
Not provided
Not provided
Not provided
Not provided
| Name | Affiliation | Role |
|---|---|---|
| LOIC MONDOLONI | Assistance Publique Hopitaux De Marseille | Study Director |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Assistance Publique Hopitaux de Marseille | Marseille | 13354 | France |
Not provided
| ID | Term |
|---|---|
| D029424 | Pulmonary Disease, Chronic Obstructive |
| ID | Term |
|---|---|
| D008173 | Lung Diseases, Obstructive |
| D008171 | Lung Diseases |
| D012140 | Respiratory Tract Diseases |
| D002908 | Chronic Disease |
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
| Determination of CO in exhaled air |
| Other |
|
| D020969 |
| Disease Attributes |
| D010335 | Pathologic Processes |
| D013568 | Pathological Conditions, Signs and Symptoms |