title: Sex-related splenocyte function in a murine model of allergic asthma.
abstract: BACKGROUND
  The prevalence and severity of asthma are higher among boys than girls, but the ratios are reversed after puberty. These observations strongly suggest that sex hormones have a role in the pathogenesis of the disease. However, the mechanisms underlying the gender differences in asthma are not fully understood.
  
  
  OBJECTIVE
  The aim of this study was to investigate sex differences in allergic inflammation in terms of immune function.
  
  
  METHODS
  Male and female C57BL/6 mice were sensitized and challenged with ovalbumin (OVA). OVA-specific IgE in serum and airway inflammation were compared between sexes. Splenocytes from OVA-sensitized male or female donor mice were transferred to male or female naïve recipient mice. Subsequently, the recipient mice were challenged, followed by the evaluation of OVA-specific IgE and airway inflammation. Cytokines secreted from splenocytes of the sensitized mice were measured.
  
  
  RESULTS
  The levels of OVA-specific IgE and the allergen-induced airway inflammation were higher in female than in the male mice. The contents of T-helper type 2 (Th2) cytokines, IL-4, IL-5 and IL-13, in the bronchoalveolar lavage fluid from female mice were higher than those from male mice. The airway inflammation in female recipients transferred with splenocytes from female donors was more severe than that in any other combination of recipients and donors. Splenocytes from the sensitized female mice produced more of the Th2 cytokine, IL-5, than those from the sensitized male mice upon stimulation with OVA.
  
  
  CONCLUSIONS
  Our findings suggest that the sex difference in allergic airway inflammation may be attributable to the sex difference in not only the hormonal environment but also in the immune cells themselves.
authors.affiliation: Department of Pathophysiology, Tohoku Pharmaceutical University, Sendai, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Okuyama
authors.forename: K
authors.initials: K
authors.lastname: Wada
authors.forename: J
authors.initials: J
authors.lastname: Chihara
authors.forename: M
authors.initials: M
authors.lastname: Takayanagi
authors.forename: I
authors.initials: I
authors.lastname: Ohno
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology*; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism; D005260:Female; D007073:Immunoglobulin E / Q000097:blood*; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D007371:Interferon-gamma / Q000276:immunology / Q000378:metabolism; D018793:Interleukin-13 / Q000096:biosynthesis / Q000276:immunology; D015847:Interleukin-4 / Q000096:biosynthesis / Q000276:immunology; D015848:Interleukin-5 / Q000096:biosynthesis / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010047:Ovalbumin / Q000276:immunology*; D012727:Sex Characteristics
chemical_list: D018793:Interleukin-13; D015848:Interleukin-5; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma; D010047:Ovalbumin