Background: Despite research into the mechanisms of injury in blast-induced thoracic trauma using animal or clinical models, some questions regarding the exact nature of such inju-ries have not been fully addressed. The present study aims to investigate the temporal altera-tions in the quantity and functions of Alveolar Macrophages (AMs) associated with intrapulmo-nary haemorrhage in a prospective rodent model of primary blast lung injury. 

Methods: Female Wister rats were randomly divided into two experimental groups: 1. the blast group, which re-ceived a single standardised blast wave; 2. the control group, which received no trauma but un-derwent the same procedure as the experimental group. AMs were harvested, cultured, and stimulated. The number of AMs was determined, and their capacity for phagocytosis, respiratory burst, and release of cytokines was determined, with or without the contribution of blood com-ponents.

Results: The number of AMs exhibited a time-dependent pattern of changes. Phagocy-tosis of dead Escherichia coli (E. coli) and superoxide production by AMs decreased 10 min and 24 h after trauma, but both parameters increased significantly 96 h after the insult. These results sug-gest a transiently impaired response of AMs to a bacterial stimulus in the initial period after thoracic trauma. However, the inclusion of blood components in the experiment further reduced the phagocytic capacity and respiratory burst of AMs. 

Conclusions: Blunt thoracic trauma in the present form and intensity impaired two important antibacterial functions of innate immunity, including the phagocytosis and superoxide generation capacity of AM and their ability to pro-duce TNF. These changes are followed by a time-dependent recovery. Alveolar haemorrhage has been shown to be at least partially involved in the impairment of the phagocytosis capacity of AMs.