This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Mammalian macrophages are known to produce reactive oxygen species during phagocytosis or stimulation by a variety of agents including ozone and aerosol sulfates. Superoxide anion and hydrogen peroxide are produced in aerobic cells either as a by-product during mitochondrial respiration or by oxidoreductases. The respiratory burst is performed by activation of NADPH oxidase and is believed to be crucial for the bactericidal action of phagocytes. Ozone exposure generally leads to respiratory burst from macrophages, and also reduction in anitoxidant activities of epithelial cells, providing one mechanism for inflammation to lung tissue. ROS and the antioxidant system has been investigated in frogs, but has not been studied in light of the innate immunity and the pulmonary system of any amphibian. This study will examine the immune defense responses to ozone and acidic sulfate aerosols in vitro exposures to toad (Bufo marinus) phagocytes. The investigator will (1) create an exposure system using viable cascade impactors to perform exposures of cells in culture, (2) establish cell culturing capability at Chaminade University, and (3) identify ROS released by amphibian macrophages. The primary objective of the work will be to establish whether ozone and or SO2 aerosols activate or suppress functional capacities of amphibian macrophages, particularly in relation to the respiratory burst and the effects on antioxidant enzymes present in the lung and whether these patterns are similar to results typical of mammalian models. Future efforts will be directed at investigating redundancy of the cytokine effects, particularly tumor necrosis factor ? alpha, leading to inflammation in non-mammalian vertebrates using amphibian macrophages as a model system.
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