CONICET | Buscador de Institutos y Recursos Humanos

Background: Obesity is characterized as the excessive accumulation of adipose tissue and represents a major cardiovascular risk factor. Clinical evidence has suggested that air pollution particulate matter (PM), an atmospheric aerosol consisting of a mixture of airborne solid particles and droplets, is a risk factor for the development of obesity and cardiometabolic disorders. However, whether direct mechanistic links between air pollution exposure and obesity exist remains unknown. Therefore, the aim of this study was to evaluate the impact of air pollution PM exposure on metabolism and obesity in mice, with special focus on unraveling pulmonary and systemic inflammatory mechanisms.Methods & Results: Male eight-week-old C57BL/6 mice were exposed to a PM surrogate (ROFA, Residual Oil Fly Ash) at 1 mg/kg body weight or PBS (control) by intranasal instillation and sacrificed at different time points. We observed inflammatory cell recruitment into the lungs and increased bronchoalveolar lavage fluid (BALF) pro-inflammatory cytokine levels (TNF-α, MCP-1, IFN-γ, IL-6), alongside an increase in pro-inflammatory gene expression, indicative of ongoing local inflammation. We also observed a sustainable increase in pro-inflammatory cytokines in plasma. In adipose tissue, we found a significant decrease in thermogenic gene expression (Ucp-1, Ppargc1a, and Adrb3) after 24 and 48 hours, suggesting a decrease in lipolysis and thermogenesis, despite ongoing adipose tissue inflammation. In order to further explore this observation, another set of mice were exposed to ROFA or PBS for 7 days and monitored in metabolic cages during 48 hours. Interestingly, despite enhanced physical activity and lowered caloric food intake, ROFA-exposed mice showed significantly reduced thermogenesis/heat production as compared to mice on PBS (p