Decreased antigen-induced eicosanoid release in conjugated linoleic acid-fed guinea pigs

• DOI: 10.1152/ajpregu.00075.2001
• Publication Date: 2015-03-03T20:24:04Z
• Authors: Leah D. Whigham; Alan Higbee; Dale E. Bjorling; Yeonhwa Park; Michael W. Pariza; Mark E. Cook
• Keywords: Hypersensitivity, Immediate; 0301 basic medicine; Ovalbumin; Prostaglandin D2; Blotting, Western; Guinea Pigs; Urinary Bladder; 6-Ketoprostaglandin F1 alpha; Dinoprost; Dinoprostone; Isoenzymes; Linoleic Acid; Trachea; 03 medical and health sciences; Cyclooxygenase 2; Prostaglandin-Endoperoxide Synthases; Animals; Eicosanoids; Female; Bronchial Hyperreactivity; Food Science

This study investigated the capacity of conjugated linoleic acids (CLA) to reduce ex vivo antigen-induced release of eicosanoids in a type I hypersensitivity model. Guinea pigs were fed a diet containing 0.25% safflower oil (control) or 0.25% CLA [43% trans( t)10, cis ( c)12; 41% c9, t11/ t9, c11 18:2] for 2 wk before and during sensitization to ovalbumin (OVA). Lungs, tracheas, and bladders were incubated in physiological saline solution (PSS) for 1 h (basal mediator release) and challenged with OVA (0.01 g/l PSS) for 1 h (mediator release in response to antigen). Eicosanoids were quantified by HPLC/tandem mass spectrometry or enzyme immunoassay. CLA feeding resulted in no change in basal release but decreased eicosanoid release from sensitized tissues in response to antigen challenge in the following manner: thromboxane B2, 6-keto-prostaglandin (PG)F1α, PGF2α, PGD2, PGE2by 57–75% in lung, 45–65% in trachea, and 38–60% in bladder; and leukotriene C4/D4/E4by 87, 90, and 50% in lung, trachea, and bladder, respectively. These data indicate that feeding CLA reduces lipid-derived inflammatory mediators produced by this type I hypersensitivity model.