The goals of this project are to define the mechanisms by which air pollution affects metabolic imbalance, identifying molecular mediators with specific emphasis on hypothalamic neuroinflammatory pathways that may ultimately have implications for potential interventions.

Volatile organic compounds (VOC), are major components of air pollution, contributing to both outdoor and indoor pollution. VOCs can enter the CNS, through direct transport or via systemic inflammation upon initial recruitment of immune cells in the lung tissue. Emerging evidence suggests that microglia and astrocytes play critical roles in the regulation of immune and inflammatory responses particles or reactive gases of urban air pollution in the CNS. Microglia, the major cell type responsible for CNS immune response, are exquisitely sensitive to stressors and are activated by inhaled components of urban air pollution through both direct and indirect pathways.

Our new studies indicate that neuroinflammatory signals of the hypothalamic glia cells are rapidly activated in response to VOC exposure and contribute to the whole-body metabolic imbalance.

Using novel genetically engineered mice models we are currently assessing the role of microglia-specific inflammatory pathway and ER stress response on the whole-body metabolism in response to VOC exposure.