Autoimmunity in Chronic Obstructive Pulmonary Disease.

Status

Active, not recruiting

Phases

Unknown

Study type

Observational

Source

NL-OMON

Registry ID

NL-OMON26251

Enrollment

120

Registered

2010-03-25

Start date

2010-04-01

Completion date

Unknown

Last updated

2024-02-28

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Chronic Obstructive Pulmonary Disease, COPD, Autoimmunity, lung, smoking, cytotoxicity, antibodies Chronische Obstructieve Bronchitis en Longemfyseem, autoimmuniteit, long, roken, cytotoxiciteit, antilichamen

Interventions

None listed

Eligibility

Inclusion criteria

Inclusion criteria: Inclusion criteria for COPD patients: 1. Clinical diagnose of COPD; 2. No allergies; 3. Post-bronchodilator FEV1 40; 5. Current or ex-smokers > 10 pack years; 6. Ex-smokers have to have quitted smoking for at least one year; 7. No other major current health problems; 8. Written informed consent. Healthy controls: 1. No signs of pulmonary disease; 2. No allergies; 3. No other major current health problems; 4. FEV1 > 90 % predicted and FEV1/FVC > 70%; 5. Age > 40; 6. Never smokers, i.e. no cigarettes last year, and 10 pack years; or ex- smokers for > 1 year and > 10 pack years; 7. Written informed consent.

Exclusion criteria

Exclusion criteria: 1. Addiction to alcohol or drugs; 2. COPD exacerbation in the 6 weeks preceding the study; 3. Immunosuppressive therapy.

Design outcomes

Primary

Measure	Time frame
1. The degree of autoantibody-mediated cytotoxicity of sera of COPD patients when compared to non-COPD patients, expressed as a fraction of cells that have died during incubation; 2. The cell types (primary bronchial epithelial cells, primary airway smooth muscle cells, primary lung fibroblasts) and cell lines (an alveolar epithelial cell line and a lung fibroblast cell line) that are primarily affected by autoantibodies as found in serum of COPD patients and healthy controls; 3. The contribution of complement, different effector cells, and antibody-free serum to the level (as outlined in the previous paragraphs) and specificity of cytotoxicity (which cells and cell lines are affected). The impact of different effector cells and antibody-free serum.	—

Measure

Time frame

1. The degree of autoantibody-mediated cytotoxicity of sera of COPD patients when compared to non-COPD patients, expressed as a fraction of cells that have died during incubation; 2. The cell types (primary bronchial epithelial cells, primary airway smooth muscle cells, primary lung fibroblasts) and cell lines (an alveolar epithelial cell line and a lung fibroblast cell line) that are primarily affected by autoantibodies as found in serum of COPD patients and healthy controls; 3. The contribution of complement, different effector cells, and antibody-free serum to the level (as outlined in the previous paragraphs) and specificity of cytotoxicity (which cells and cell lines are affected). The impact of different effector cells and antibody-free serum.

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Secondary

Measure	Time frame
1. Effects of age, aspects of smoking history, clinical and immunological parameters on cytotoxicity; 2. Insight into the components which play a role in lung remodelling and destruction. We expect that results will lead to more attention for COPD and more focus on relevant targets in drug development programs; 3. A better understanding of the mechanisms underlying the pathological changes in lungs of patients with COPD, and identification of characteristics of patients which may benefit from anti-autoimmune therapy. This is necessary to be able to develop more targeted drug development programs and to develop efficient therapies; 4. Due to the similarities of COPD to other autoimmune disease (outlined above), opportunities for improved treatment and medication may in part be based on regimes used in other autoimmune diseases.	—

Measure

Time frame

1. Effects of age, aspects of smoking history, clinical and immunological parameters on cytotoxicity; 2. Insight into the components which play a role in lung remodelling and destruction. We expect that results will lead to more attention for COPD and more focus on relevant targets in drug development programs; 3. A better understanding of the mechanisms underlying the pathological changes in lungs of patients with COPD, and identification of characteristics of patients which may benefit from anti-autoimmune therapy. This is necessary to be able to develop more targeted drug development programs and to develop efficient therapies; 4. Due to the similarities of COPD to other autoimmune disease (outlined above), opportunities for improved treatment and medication may in part be based on regimes used in other autoimmune diseases.

—

Contacts

Public ContactJoost Wessels

j.r.l.wessels@bvl.umcg.nl+31 (0)50 3614464

Outcome results