title: Oral-tolerance induction in diet-induced obese mice.
abstract: OBJECTIVE
  It is known that immune functions are altered in various ways by obesity. However, changes in the intestinal immune system resulting from obesity remain poorly understood. Oral tolerance is a system that suppresses antigen specific immune responses to orally administrated antigens. The intestinal immune system is intimately associated with the oral tolerance system, that acts to prevent allergic and inflammatory diseases. In this study we investigated the effect of obesity on induction of oral tolerance to ovalbumin (OVA) in an animal model of obesity.
  
  
  METHODS
  Obese mice induced by a high fat diet and control mice were allowed free access for 3 days to a 1%-ovalbumin (OVA) solution in drinking water. After continuous feeding of the antigen, all the mice were immunized by two intraperitoneal injections of OVA administered 7 days apart.
  
  
  RESULTS
  In the control mice, induction of oral tolerance caused an increase in antigen specific IgG1 levels and a decrease in IgG2a levels. In contrast, the IgG1/IgG2a ratio was reversed in obese mice. OVA-specific IL-2 production was suppressed by antigen feeding in both the control and obese mice; however, suppression of OVA-specific IL-10 was observed only in the control mice. Although OVA-specific IgA and IgM were not affected by antigen feeding, the obese groups of mice had significantly lower titers of antibodies.
  
  
  CONCLUSIONS
  These findings suggest that obesity may affect induction of oral tolerance following antigen feeding and that these changes may be related to the inflammatory reaction.
authors.affiliation: Division of Applied Food Research, National Institute of Health and Nutrition, 1-23-1, Toyama, Shinjuku-ku, Tokyo 162-8636, Japan. himawari@nih.go.jp
authors.forename: Natsuko
authors.initials: N
authors.lastname: Mito
authors.forename: Tomoko
authors.initials: T
authors.lastname: Kaburagi
authors.forename: Haruka
authors.initials: H
authors.lastname: Yoshino
authors.forename: Atsuko
authors.initials: A
authors.lastname: Imai
authors.forename: Kazuto
authors.initials: K
authors.lastname: Sato
mesh_terms: D000818:Animals; D000941:Antigens / Q000008:administration & dosage / Q000276:immunology; D004032:Diet; D004041:Dietary Fats / Q000633:toxicity; D007108:Immune Tolerance; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D016753:Interleukin-10 / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D051379:Mice; D009055:Mouth / Q000276:immunology*; D009765:Obesity / Q000139:chemically induced / Q000276:immunology*; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D013154:Spleen / Q000166:cytology / Q000276:immunology
chemical_list: D000941:Antigens; D004041:Dietary Fats; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007376:Interleukin-2; D016753:Interleukin-10; D015847:Interleukin-4; D010047:Ovalbumin