Oxidative stress and macrophages: driving forces behind exacerbations of asthma and chronic obstructive pulmonary disease?

Oxidative stress is a common feature of obstructive airway diseases like asthma and chronic obstructive pulmonary disease (COPD). Lung macrophages are key innate immune cells that can generate oxidants and are known to display aberrant polarization patterns and defective phagocytic responses in thes...

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Bibliographic Details
Published in:American journal of physiology. Lung cellular and molecular physiology 2019-02, Vol.316 (2), p.L369-L384
Main Authors: de Groot, Linsey E S, van der Veen, T Anienke, Martinez, Fernando O, Hamann, Jörg, Lutter, René, Melgert, Barbro N
Format: Article
Language:English
Subjects:
Asthma
Asthma - immunology
Chronic obstructive pulmonary disease
Humans
Immune system
Inflammation - immunology
Lung diseases
Macrophages
Macrophages - immunology
Macrophages, Alveolar - immunology
Obstructive lung disease
Oxidants
Oxidation
Oxidative stress
Oxidative Stress - physiology
Oxidizing agents
Phagocytes
Pulmonary Disease, Chronic Obstructive - immunology
Respiratory tract diseases
State-of-the-art reviews
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Summary:Oxidative stress is a common feature of obstructive airway diseases like asthma and chronic obstructive pulmonary disease (COPD). Lung macrophages are key innate immune cells that can generate oxidants and are known to display aberrant polarization patterns and defective phagocytic responses in these diseases. Whether these characteristics are linked in one way or another and whether they contribute to the onset and severity of exacerbations in asthma and COPD remain poorly understood. Insight into oxidative stress, macrophages, and their interactions may be important in fully understanding acute worsening of lung disease. This review therefore highlights the current state of the art regarding the role of oxidative stress and macrophages in exacerbations of asthma and COPD. It shows that oxidative stress can attenuate macrophage function, which may result in impaired responses toward exacerbating triggers and may contribute to exaggerated inflammation in the airways.
ISSN:1040-0605
1522-1504
DOI:10.1152/ajplung.00456.2018