Chemical exposure and alveolar macrophages responses: 'the role of pulmonary defense mechanism in inhalation injuries'

Abstract

Epidemiological and clinical studies have indicated an association between particulate matter (PM) exposure and acute and chronic pulmonary inflammation, which may be registered as increased mortality and morbidity. Despite the increasing evidence, the pathophysiology mechanism of these PMs is still not fully characterised. Pulmonary alveolar macrophages (PAMs), as a predominant cell in the lung, play a critically important role in these pathological mechanisms. Toxin exposure triggers events associated with macrophage activation, including oxidative stress, acute damage, tissue disruption, remodelling and fibrosis. Targeting macrophage may potentially be employed to treat these types of lung inflammation without affecting the natural immune response to bacterial infections. Biological toxins, their sources of exposure, physical and other properties, and their effects on the individuals are summarised in this article. Inhaled particulates from air pollution and toxic gases containing chemicals can interact with alveolar epithelial cells and immune cells in the airways. PAMs can sense ambient pollutants and be stimulated, triggering cellular signalling pathways. These cells are highly adaptable and can change their function and phenotype in response to inhaled agents. PAMs also have the ability to polarise and undergo plasticity in response to tissue damage, while maintaining resistance to exposure to inhaled agents.