title: Nutritional regulation of porcine bacterial-induced colitis by conjugated linoleic acid.
abstract: Excessive intake of saturated fatty acids and/or linoleic acid favors the induction of an array of lipid mediators and cytokines enhancing inflammatory responses. Conversely, dietary supplementation with (n-3) fatty acids or vitamin D ameliorates inflammation and autoimmune diseases. Although it was well accepted that conjugated linoleic acid (CLA) prevented diseases with a common inflammatory pathogenesis (i.e., cancer and atherosclerosis), no studies were available on the roles of CLA in mucosal inflammation. The present study was designed to investigate the anti-inflammatory actions and molecular mechanisms underlying the regulation of colonic health by CLA. We hypothesized that colonic inflammation can be ameliorated by dietary CLA supplementation. To test this hypothesis, inflammation of the colonic mucosa was triggered by challenging pigs fed either soybean oil-supplemented or CLA-supplemented diets with an enteric bacterial pathogen (i.e., Brachyspira hyodysenteriae). Immunoregulatory cytokines and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) mRNA expression were assayed in colonic lymph nodes and colon of pigs. Colonic mucosal lesions and lymphocyte subset distribution were evaluated by histology and immunohistochemistry. Supplementation of CLA in the diet before the induction of colitis decreased mucosal damage; maintained cytokine profiles (i.e., interferon-gamma and interleukin-10) and lymphocyte subset distributions (i.e., CD4+ and CD8+), resembling those of noninfected pigs; enhanced colonic expression of PPAR-gamma; and attenuated growth failure. Therefore, CLA fed preventively before the onset of enteric disease attenuated inflammatory lesion development and growth failure.
authors.affiliation: Veterinary Medical Research Institute, Nutritional Immunology, College of Veterinary Medicine, Ames, IA 50011, USA.
authors.forename: Raquel
authors.initials: R
authors.lastname: Hontecillas
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Wannemeulher
authors.forename: Dean R
authors.initials: DR
authors.lastname: Zimmerman
authors.forename: David L
authors.initials: DL
authors.lastname: Hutto
authors.forename: Jennifer H
authors.initials: JH
authors.lastname: Wilson
authors.forename: Dong U
authors.initials: DU
authors.lastname: Ahn
authors.forename: Josep
authors.initials: J
authors.lastname: Bassaganya-Riera
mesh_terms: D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D003092:Colitis / Q000382:microbiology* / Q000473:pathology / Q000517:prevention & control*; D003106:Colon / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000235:genetics; D004032:Diet; D004041:Dietary Fats / Q000008:administration & dosage; D005227:Fatty Acids / Q000008:administration & dosage; D006130:Growth Disorders / Q000209:etiology; D007413:Intestinal Mucosa / Q000473:pathology; D019787:Linoleic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D016131:Lymphocyte Subsets / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics; D013145:Spirochaetales Infections / Q000150:complications; D013552:Swine; D013553:Swine Diseases; D014157:Transcription Factors / Q000235:genetics
chemical_list: D016207:Cytokines; D004041:Dietary Fats; D005227:Fatty Acids; D012333:RNA, Messenger; D018160:Receptors, Cytoplasmic and Nuclear; D014157:Transcription Factors; D019787:Linoleic Acid