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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
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Oxidative stress decreases functional airway mannose binding lectin in COPD
Hai B Tran1, Jessica Ahern1, Greg Hodge2
1Lung Research, Hanson Institute and Department Thoracic Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia.
Plos One
|June 6, 2014
Summary
Oxidative stress damages mannose binding lectin (MBL) in COPD airways, impairing macrophage efferocytosis and pathogen clearance. This MBL dysfunction offers a new therapeutic target for chronic obstructive pulmonary disease (COPD).
Area of Science:
- Pulmonary immunology
- Oxidative stress research
- Macrophage biology
Background:
- Alveolar macrophages (AM) dysfunction in efferocytosis and pathogen clearance is a therapeutic target in COPD.
- Mannose binding lectin (MBL) levels are reduced in COPD airways, impacting macrophage function.
- Increased airway oxidative stress may cause MBL disturbances.
Purpose of the Study:
- To investigate the effects of oxidation on MBL structure and function.
- To assess MBL's interaction with macrophages under oxidative stress.
- To explore MBL as a therapeutic target in COPD.
Main Methods:
- Oxidation of plasma-derived MBL (pdMBL) using AAPH.
- Analysis of MBL oligomeric structure via blue native PAGE.
- Assessment of macrophage efferocytosis, NTHi phagocytosis, and scavenger receptor expression (SRA1) with pdMBL and oxidized MBL (oxMBL).
Main Results:
- Oxidation disrupted MBL oligomeric structure.
- OxMBL significantly reduced macrophage phagocytosis of apoptotic cells and NTHi compared to pdMBL.
- Oxidation abrogated the MBL-induced increase in macrophage scavenger receptor 1 (SRA1) expression.
Conclusions:
- Pulmonary macrophage dysfunction in COPD may stem from oxidative stress-induced MBL damage.
- Oxidized MBL impairs crucial macrophage functions.
- Targeting MBL in COPD presents a potential therapeutic strategy.
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