title: Impaired contact hypersensitivity in diet-induced obese mice.
abstract: BACKGROUND
  Epidemiological studies suggest that obesity is associated with the impairment of immunity. However, there is no experimental evidence that obesity prejudices immune responses.
  
  
  OBJECTIVE
  This study was designed to determine the effects of obesity on contact hypersensitivity (CHS) response using a diet-induced obese (DIO) mouse model.
  
  
  METHODS
  The effect of high fat diet (HFD) on CHS response to trinitrochlorobenzene (TNCB) was assessed by ear swelling, cytokine production, functional analysis of epidermal Langerhans cells, and adoptive transfer of immune cells. Immune response to ovalbumin was also analyzed in DIO mice.
  
  
  RESULTS
  C57BL/6 mice but not BALB/c mice that fed with HFD for 4 weeks or more became obese and showed impaired CHS response, although both strain of mice showed enhanced irritant response to TNCB. CHS response was slightly impaired when C57BL/6 mice fed with HFD for 1 or 2 weeks. This suggests that diet-induced obesity or the HFD itself impairs the CHS response in the susceptible mice. The adoptive transfer of immune cells from DIO mice sensitized with TNCB to naïve mice failed to show vigorous CHS, which suggests dysfunction of an afferent phase of CHS in DIO mice. However, the number and allo-stimulating ability of epidermal Langerhans cells were comparable between DIO mice and lean mice. In addition, the immune response to ovalbumin (delayed type hypersensitivity, and antigen-dependent production of antibodies and cytokine) was preserved in DIO mice.
  
  
  CONCLUSIONS
  These results suggest that the diet-induced obesity or the HFD only partially impairs immunity in the susceptible mice.
authors.affiliation: Department of Anatomy, Faculty of Medicine, Oita University, Idaigaoka 1-1, Hasama-machi, Oita 879-5593, Japan. katagiri@med.oita-u.ac.jp
authors.forename: Kazumoto
authors.initials: K
authors.lastname: Katagiri
authors.forename: Shoko
authors.initials: S
authors.lastname: Arakawa
authors.forename: Rieko
authors.initials: R
authors.lastname: Kurahashi
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Hatano
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D017449:Dermatitis, Allergic Contact / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D004041:Dietary Fats; D004195:Disease Models, Animal; D004487:Edema / Q000276:immunology; D005260:Female; D006968:Hypersensitivity, Delayed / Q000139:chemically induced / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D007801:Langerhans Cells / Q000276:immunology; D020738:Leptin / Q000097:blood; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000097:blood / Q000139:chemically induced / Q000150:complications / Q000276:immunology*; D010047:Ovalbumin; D010853:Picryl Chloride; D013045:Species Specificity; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000637:transplantation; D013997:Time Factors
chemical_list: D016207:Cytokines; D004041:Dietary Fats; D020738:Leptin; D010047:Ovalbumin; D010853:Picryl Chloride