The Role and Phagocytic Mechanisms of Alveolar Macrophages in Inflammatory Responses Induced by Diesel Exhaust Particles

This is the authors' abstract. We don't add key points for this paper.

Alveolar macrophages, the most abundant innate immune cells in the distal lung parenchyma, are not only essential for maintaining pulmonary homeostasis but also orchestrate pulmonary and thus systemic responses to ambient particulate matter. However, their specific role in the development of adverse health effects related to ambient fine particulate matter (PM 2.5 ) exposure remains insufficiently understood. In this study, we used both mouse models and cultured cells to document their role in the development of pulmonary inflammation due to exposure to diesel exhaust particles (DEP), the main component of urban PM 2.5 . The results revealed that DEP induced pulmonary inflammation as well as an acute phase response in the lung and liver within 24 h, which gradually diminished over the subsequent week. Depletion of alveolar macrophages alleviated the DEP-induced pulmonary inflammation and acute phase response. Furthermore, this study showed that Msr1 may be the primary receptor responsible for the phagocytosis of DEP in macrophages, while the PIP2-mediated nonbiological phagocytic signaling pathway appeared to be nonsignificant. All of the results in the present study reveal the key role of alveolar macrophages in DEP-induced pulmonary inflammation, enhancing our understanding of the complex interactions among DEP, alveolar macrophages, and inflammatory responses.