UC San Diego

Exposure to burn pits during deployment has been linked to lung injury and illnesses in U.S. Army personnel that served in Iraq and Afghanistan. Despite this existing correlation, there is a lack of models to study the effects of short-term burn pit exposure and its mechanisms leading to its pathogenicity. In addition, how inhalation of burn pit combustion products (BPC) affects the immunity of the lungs remains unclear. In this thesis, we present an acute murine model that simulates inhalation of known constituents present in burn pit exposures and analyze the affected lung tissues using flow cytometry to investigate changes in innate immune cells. Our findings show that this model successfully induces neutrophilic lung inflammation that may be similar to that observed in individuals affected by BPC. Mice exposed to BPC in combination with the fungal allergen Alternaria induced neutrophilia in addition to type 2 eosinophilic inflammation. BPC exposure led to the suppression of Group 2 Innate lymphoid cells (ILC2s) and an increase in ILC1-like cells. Our preliminary studies show that Stimulator of interferon genes (STING) pathway may be required for BPC-induced neutrophilia. Our results suggest that inflammation type shift following burn pit exposure may be ILC1 mediated and regulated through STING, though further studies are needed to fully understand the underlying molecular mechanisms behind the changes in innate immunity. Overall, this study could provide insights into the effects of burn pit exposure on lung immune responses and may lead to the development of interventions for burn pit-exposed personnel.