title: Two opposite extremes of adiposity similarly reduce inflammatory response of antigen-induced acute joint inflammation.
abstract: OBJECTIVE
  Acute inflammation is a normal response of tissue to an injury. During this process, inflammatory mediators are produced and metabolic alterations occur. Adipose tissue is metabolically activated, and upon food consumption, it disrupts the inflammatory response. However, little is known about the acute inflammatory response in joints that results from diet-induced adipose tissue remodeling. The objective of this study was to determine whether alterations in adipose tissue mass arising from food consumption modify the inflammatory response of antigen-induced joint inflammation in mice.
  
  
  METHODS
  Male BALB/c mice were fed a chow diet, a highly refined carbohydrate-containing (HC) diet for 8 wk. They were then immunized and, after 2 wk, received a knee injection of methylated bovine serum albumin (mBSA). They were sacrificed at 6, 24, and 48 h after injection. The effect of the cafeteria diet for 8 wk, which also increases adipose tissue, or conjugated linoleic acid (CLA) supplementation for 4 wk, a model of lipodystrophy, was evaluated 24 h after knee challenge with mBSA.
  
  
  RESULTS
  Cellular influx, predominantly neutrophils, in synovial fluid was attenuated in the HC diet group, as were levels of myeloperoxidase and IL-1β in periarticular tissue and histopathological analysis. These responses were associated with reduced adiponectin and increased leptin in serum, which was pronounced in mice fed the HC diet. Cafeteria diet and CLA supplementation induced a profile similar to that seen with the HC diet in terms of inflammation, disease response, and metabolic alteration. Interestingly, after the injection of mBSA, the area of adipocytes in the infrapatellar fat pad increased in mice fed with chow diet similar to those fed the HC and cafeteria diet.
  
  
  CONCLUSIONS
  We demonstrated that attenuation of joint response induced by diet was independent of adipose tissue remodeling but could be associated with metabolic alterations.
authors.affiliation: Nutrition Department, Nursing School, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil; Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Marina Chaves de
authors.initials: MC
authors.lastname: Oliveira
authors.affiliation: Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Ana Letícia Malheiros
authors.initials: AL
authors.lastname: Silveira
authors.affiliation: Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Luciana Pádua
authors.initials: LP
authors.lastname: Tavares
authors.affiliation: Nutrition Department, Nursing School, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Débora Fernandes
authors.initials: DF
authors.lastname: Rodrigues
authors.affiliation: Experimental Rheumatology, Radboud university medical center, Nijmegen, the Netherlands.
authors.forename: Fons A J
authors.initials: FA
authors.lastname: van de Loo
authors.affiliation: Department of Clinical and Toxicological Analyses, Faculty of Pharmacy, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Lirlândia Pires de
authors.initials: LP
authors.lastname: Sousa
authors.affiliation: Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Mauro Martins
authors.initials: MM
authors.lastname: Teixeira
authors.affiliation: Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Flávio Almeida
authors.initials: FA
authors.lastname: Amaral
authors.affiliation: Nutrition Department, Nursing School, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil; Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Electronic address: Adaliene@gmail.com.
authors.forename: Adaliene Versiani Matos
authors.initials: AV
authors.lastname: Ferreira
mesh_terms: D017667:Adipocytes; D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology; D050154:Adiposity; D000818:Animals; D001168:Arthritis / Q000139:chemically induced / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D004032:Diet; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000378:metabolism; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism; D019587:Dietary Supplements; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism*; D053583:Interleukin-1beta / Q000097:blood; D007719:Knee Joint / Q000378:metabolism / Q000473:pathology; D020738:Leptin / Q000097:blood; D044243:Linoleic Acids, Conjugated / Q000494:pharmacology; D050356:Lipid Metabolism; D008060:Lipodystrophy / Q000150:complications / Q000378:metabolism*; D008297:Male; D055442:Metabolome; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000378:metabolism; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D009195:Peroxidase / Q000097:blood; D012710:Serum Albumin, Bovine
chemical_list: D052242:Adiponectin; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D053583:Interleukin-1beta; D020738:Leptin; D044243:Linoleic Acids, Conjugated; D012710:Serum Albumin, Bovine; D009195:Peroxidase
keywords: Adipocytes; Arthritis; Diet; Inflammation; Metabolism