Aging affects immune function, increasing an organism’s vulnerability to infectious and neoplastic diseases, however efforts in medical research have focused on adaptive immunity, leaving the role of innate immunity largely open for investigation. Echinoderms are an excellent model for studying innate immunity as invertebrates lacking adaptive immunity and as deuterosomes being more closely related to humans than any other invertebrate group. A survey of the immune gene repertoire encoded by the sea urchin genome reveals enormous and unprecedented complexity and it has been hypothesized that the robust innate immune system may play a role in both the longevity and resistance to disease that these animals exhibit.

It has been shown that inhaled particulate matter such as air pollution and asbestos are linked to a number of immune diseases such as asthma, and Systemic Lupus Erythematosus (SLE), respectively. This research may contribute to understanding the mechanisms of how asbestos and air pollution particulate (PM10) produce oxidative stress on macrophages, as well as how the macrophages will respond to the oxidative stressors. Using Flow Cytometry, DCFDA Fluorescence, Glutamate Transport, and Cytokine Bead Array assays, we have shown that exposure to asbestos and PM10 up-regulates system xc- in macrophages, which reduces oxidative stress for the macrophage by providing substrates for antioxidants. The results demonstrate that asbestos, but not PM10, induces both expression and activity of system xc-.