title: Female mice are more susceptible to the development of allergic airway inflammation than male mice.
abstract: BACKGROUND
  In humans the prevalence of asthma is higher among females than among males after puberty. The reason for this phenomenon is not clear.
  
  
  OBJECTIVE
  We tested the hypothesis that female mice are more susceptible to the development of allergic asthma than male mice and studied allergic immune responses in the lung.
  
  
  METHODS
  We compared allergic airway inflammation, i.e. methacholine (MCh) responsiveness, serum IgE, and cytokines, and the number of the different leucocytes in lungs of male and female BALB/c mice, twice-sensitized to ovalbumin (OVA) and subsequently challenged with OVA (OVA-mice) or phosphate-buffered saline (PBS-mice) aerosols on days 24-26, 30, and 31.
  
  
  RESULTS
  OVA challenge significantly increased MCh responsiveness, numbers of eosinophils, CD4(+) T cells, CD4(+)/CD25(+) T cells, B cells, and levels of Thelper (Th)2 cytokines, total, and OVA-specific IgE. There was, however, also an effect of gender, with female mice responding to OVA challenges with higher numbers of eosinophils, CD4(+) T cells, B cells, and levels of IL-4, IL-13, IFN-gamma, total, and OVA-specific IgE than male mice. In contrast, female PBS-mice had significantly lower percentages of regulatory CD4(+)/CD25(+) T cells than males (females 4.2+/-0.2% vs. males 5.3+/-0.1% of CD4(+) T cells, P<0.05).
  
  
  CONCLUSIONS
  Female mice develop a more pronounced type of allergic airway inflammation than male mice after OVA challenge. The reduced percentage of regulatory T cells in the lungs of female PBS-mice may indicate that the level of these cells in the lung during the sensitization phase is important for the development and/or progression of an allergic immune response after multiple OVA challenges.
authors.affiliation: Department of Pathology and Laboratory Medicine, University Hospital Groningen, Groningen, The Netherlands. B.N.Melgert@path.umcg.nl
authors.forename: B N
authors.initials: BN
authors.lastname: Melgert
authors.forename: D S
authors.initials: DS
authors.lastname: Postma
authors.forename: I
authors.initials: I
authors.lastname: Kuipers
authors.forename: M
authors.initials: M
authors.lastname: Geerlings
authors.forename: M A
authors.initials: MA
authors.lastname: Luinge
authors.forename: B W A
authors.initials: BW
authors.lastname: van der Strate
authors.forename: H A M
authors.initials: HA
authors.lastname: Kerstjens
authors.forename: W
authors.initials: W
authors.lastname: Timens
authors.forename: M N
authors.initials: MN
authors.lastname: Hylkema
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology; D001402:B-Lymphocytes / Q000276:immunology; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D015704:CD4 Antigens / Q000276:immunology; D018946:Chemokine CCL5 / Q000032:analysis; D004804:Eosinophils / Q000276:immunology; D005260:Female; D007073:Immunoglobulin E / Q000032:analysis; D007378:Interleukins / Q000032:analysis; D008168:Lung / Q000276:immunology* / Q000473:pathology; D008297:Male; D016210:Methacholine Chloride / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D015375:Receptors, Interleukin-2 / Q000276:immunology; D012737:Sex Factors; D013601:T-Lymphocytes / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D015704:CD4 Antigens; D018946:Chemokine CCL5; D007378:Interleukins; D015375:Receptors, Interleukin-2; D016210:Methacholine Chloride; D007073:Immunoglobulin E; D010047:Ovalbumin