Cigarette smoke exposure and alveolar macrophages: mechanisms for lung disease
Research output: Contribution to journal › Review article › peer-review
Colleges, School and Institutes
Cigarette smoking is the leading cause of preventable death worldwide. It causes chronic lung disease and predisposes individuals to acute lung injury and pulmonary infection. Alveolar macrophages are sentinel cells strategically positioned in the interface between the airway lumen and the alveolar spaces. These are the most abundant immune cells and are the first line of defence against inhaled particulates and pathogens. Recently there has been a better understanding about the ontogeny, phenotype and function of alveolar macrophages and their role, not only in phagocytosis, but also in initiating and resolving immune response. Many of the functions of the alveolar macrophage have been shown to be dysregulated following exposure to cigarette smoke. Whilst the mechanisms for these changes remain poorly understood, they are important in the understanding of cigarette smoking induced lung disease. We review the mechanisms by which smoking affects alveolar macrophage: (i) recruitment, (ii) phenotype, (iii) immune function (bacterial killing, phagocytosis, proteinase/anti-proteinase release and reactive oxygen species production) and (iv) homeostasis (surfactant/lipid processing, iron homeostasis, and efferocytosis). Further understanding of the mechanisms of cigarette smoking on alveolar macrophages and other lung monocyte/macrophage populations may allow novel ways of restoring cellular function in those patients who have stopped smoking in order to reduce the risk of subsequent infection or further lung injury.
|Early online date||13 May 2021|
|Publication status||E-pub ahead of print - 13 May 2021|