Air Pollution and Neuroinflammation

Air pollution consists of a complex mixture of chemicals, particular matter (PM), organic compounds, metals, ions, and elemental carbon, which can harm living organisms, including humans. The several PM adverse effects may relate to its physicochemical characteristics, including mass, size, number, surface area, concentration, source, and composition. Since the last decade, the central nervous system (CNS) has also been proposed to be a target organ for the detrimental effects of airborne pollutants. Emerging evidence from epidemiological, clinical, and experimental studies suggest that certain neurological diseases, such as Alzheimer’s disease, may be strongly associated with ambient air pollution. Although the precise mechanisms underlying neurodegenerative diseases still remain elusive and are not fully understood, environmental pollution is believed to exert its neurotoxic function through oxidative stress, glial activation, and cerebrovascular damage. The aim of our study is to explore the effects of airborne pollution on CNS elements and brain homeostasis focusing on microglia, brain cells of nonneural origin, as predominant regulators of neuroinflammation. To explore the effects of airborne pollution on microglia we treated, at different timepoints, an immortalized line of murine microglia (i.e., BV2) with different concentration of a standard reference material of diesel exhaust particles (DEP), one of the main component of airborne pollutants at urban area. After the treatment, we evaluated cell viability, cell morphology, and intracellular calcium waves by means of calcium imaging technique. Our preliminary data suggest that BV2 cells actively interact with DEP after 24 h treatment. DEP seems to be also chemoattractant factor for BV2, but the exact mechanisms are still unknown. We are going to deeply investigate how DEP is able to interact with BV2 functions, thus triggering neuroinflammation and neurodegeneration.