Talk abstracts
Talk on Tuesday 03:30-03:45pm submitted by Hannah Lovins
Eicosapentaenoic Acid Improves Ozone-Induced Airspace Inflammation through an Oxylipin-Mediated Mechanism
Hannah B. Lovins (Molecular, Cellular, and Developmental Biology Graduate Program), Anushka Mehta, Evie Schott, Sam Cochran, Grace Hutton, Michael Yaeger (Division of Pulmonary, Critical Care and Sleep Medicine, OSU Wexner Medical Center, Columbus, OH ), Brita Kilburg-Basnyat (Arcus Biosciences, Hayward, CA), Saame Raza Shaikh (Department of Nutrition, Gillings School of Global Public Health and School of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill NC USA), Kymberly M. Gowdy (Division of Pulmonary, Critical Care and Sleep Medicine, OSU Wexner Medical Center, Columbus, OH )
Abstract:
The air pollutant ozone (O3) exacerbates chronic lung diseases. O3 activates inflammation with metabolism of n-6 polyunsaturated fatty acids (PUFAs), such as Arachidonic Acid (AA). N-6 PUFAs include inflammatory prostaglandins (PG), leukotrienes (LT), and thromboxanes (TX). It is unknown if PUFA metabolism is the mechanism where O3 exacerbates lung diseases. Diet modulates the response to O3. Mediterranean Diet, rich in n-3 PUFAs, decreases health effects from O3 exposure, but a dietary component driving this is currently unknown. Eicosapentaenoic Acid (EPA), an n-3 PUFA, lowers inflammation through conversion to 5,12,or18-HydroxyEPA (5,12,18-HEPE). We hypothesize increased dietary EPA will decrease O3-induced inflammation by promoting EPA-derived metabolites in the lung.
Mice were fed control or EPA-supplemented diet for 4 weeks, exposed to filtered air or O3 and euthanized 24hrs post O3 where bronchoalveolar lavage fluid was collected to assess airspace inflammation/injury and lung tissue for targeted LC/MS lipidomics.
Post O3, mice fed EPA-supplementation had significantly less inflammation with fewer neutrophils. However, EPA did not affect lung injury following O3. LC-MS lipidomics showed EPA increased pulmonary synthesis of EPA-derived metabolites 5, 12, and 15-HEPE, 17,18-Epoxyeicosatetraenoic Acid (17,18-EpETE), and 17,18-Dihydroxyeicosatetraenoic Acid (17,18-DiHETE). Additionally, EPA supplementation decreased generation of pro-inflammatory AA-derived metabolites LTB4, PGE2, and TXB2.
Together, results indicate EPA protects from O3-induced inflammation at cellular levels. However, EPA supplementation did not protect from O3-induced lung injury. EPA supplementation decreased AA metabolites, reducing inflammation and promoting resolution through EPA metabolism following O3 exposure. Future studies will investigate the mechanism by which EPA supplementation protects from O3-induced inflammation by utilizing 5 and 12-HEPE add-back experiments.
Keywords: Nutrition, Air Pollution, Omega-3 Polyunsaturated Fatty Acids