Acceleration of acute lung inflammation by IL-1α released through cell death of alveolar macrophages upon phagocytosis of fine Asian sand dust particles.

Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating respiratory diseases. Despite this, the intricate physiological responses triggered by inhaled ASD particles remain incompletely understood. This study aimed to comprehensively examine the respiratory effects of ASD, focusing on the spatial distribution of inhaled ASD fine particles within the lungs and the immediate physiological responses they incite. Intratracheal administration of ASD fine particles in mice resulted in efficient phagocytosis by alveolar macrophages (AMs), leading to subsequent neutrophilic inflammation. A subset of ASD-phagocytosed AMs underwent necroptosis, releasing interleukin-1α (IL-1α), causing an increase in chemokines and neutrophils. These responses occurred rapidly within hours of exposure, with endotoxin in ASD particles contributing to the process. Despite variations in desert sand dust composition based on collection locale and timing, this study's findings provide a foundational basis for understanding the biological effects of desert sand dust. Insights gained into the biological responses to desert sand dust hold promise for developing preventive measures such as air purifiers, and therapeutic agents such as IL-1α neutralizing antibodies, antibacterial agents and cell death inhibitors for human diseases associated with such environmental exposures.