Research Article Advance Publication
Effect of Exposure to Atmospheric Ultrafine Particles on Production of Free Fatty Acids and Lipid Metabolites in the Mouse Small Intestine
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Citation: Li R, Navab K, Hough G, Daher N, Zhang M, Mittelstein D, Lee K, Pakbin P, Saffari A, Bhetraratana M, Sulaiman D, Beebe T, Wu L, Jen N, Wine E, Tseng CH, Araujo JA, Fogelman A, Sioutas C, Navab M, Hsiai TK. Effect of Exposure to Atmospheric Ultrafine Particles on Production of Free Fatty Acids and Lipid Metabolites in the Mouse Small Intestine. Environ Health Perspect; http://dx.doi.org/10.1289/ehp.1307036.
Received: 2 May 2013
Accepted: 27 August 2014
Advance Publication: 29 August 2014
Background and Objective: Exposure to ambient ultrafine particulate matter (UFP) is a well-recognized risk factor for cardiovascular and respiratory diseases. However, little is known about the effects of air pollution on gastrointestinal disorders. We sought to assess whether exposure to ambient ultrafine particles (UFP: diameter < 180 nm) increased free fatty acids and lipid metabolites in the mouse small intestine.
Methods and Results: LDLR-null mice were exposed to filtered air (FA) or UFP collected at an urban Los Angeles site heavily impacted by vehicular emissions for 10 weeks in the presence or absence of D-4F, an apolipoprotein A-I mimetic peptide with anti-oxidant and anti-inflammation properties on a high-fat or normal chow diet. Compared to FA, exposure to UFP significantly increased intestinal hydroxyeicosatetraenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic acids (HODEs), including 13-HODE and 9-HODE. Arachidonic acid and prostaglandin D2 (PGD2) as well as some of the lysophosphatidic acids (LPA) in the small intestine were also increased in response to UFP exposure. Administration of D-4F significantly reduced UFP-mediated increase in HETES, HODEs, AA, PGD2 and LPA. While exposure to UFP further led to shortened villus length accompanied by prominent macrophage and neutrophil infiltration into the intestinal villi, administration of D-4F mitigated macrophage infiltration.
Conclusions: Exposure to UFP promotes lipid metabolism, villus shortening and inflammatory responses in mouse small intestine, whereas administration of D-4F attenuated these effects. Our findings provide a basis to further assess the mechanisms underlying UFP-mediated lipid metabolism in the digestive system with clinical relevance to gut homeostasis and diseases.
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