title: Gender difference in allergic airway remodelling and immunoglobulin production in mouse model of asthma.
abstract: OBJECTIVE
  Epidemiological studies have shown that the prevalence of adult asthma and severe asthma is higher in women. It has also been reported that female mice are more susceptible than males to the development of allergic airway inflammation and airway hyperresponsiveness (AHR). The influence of gender difference in the pathogenesis of severe asthma, especially airway remodelling in an animal model, has been studied rarely. We investigated gender difference in the development of airway remodelling using a long-term antigen-challenged mouse asthma model.
  
  
  METHODS
  Following ovalbumin (OVA)/alum intraperitoneal injection, male or female mice (BALB/c) were challenged with aerosolized 1% OVA on 3 days/week for 5 weeks, and differences in AHR, airway inflammation and airway remodelling between the sexes were investigated.
  
  
  RESULTS
  In OVA-sensitized and OVA-challenged (OVA/OVA) female mice, eosinophils, lymphocytes, T-helper type 2 cytokines and growth factors in bronchoalveolar lavage fluid were increased compared with OVA/OVA male mice. Histological features of airway remodelling were also increased in OVA/OVA female mice. Serum total and OVA-specific immunoglobulin E (IgE) and serum IgA were significantly elevated in OVA/OVA female mice.
  
  
  CONCLUSIONS
  These results indicate that female mice experience more airway remodelling compared with male mice. These results suggest the involvement of sex hormones and gender differences in cellular functions in airway remodelling.
authors.affiliation: Department of Infection, Allergy, Clinical Immunology and Laboratory Medicine, Akita University Graduate School of Medicine, Akita.
authors.forename: Masahide
authors.initials: M
authors.lastname: Takeda
authors.forename: Masako
authors.initials: M
authors.lastname: Tanabe
authors.forename: Wataru
authors.initials: W
authors.lastname: Ito
authors.forename: Shigeharu
authors.initials: S
authors.lastname: Ueki
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Konnno
authors.forename: Mami
authors.initials: M
authors.lastname: Chihara
authors.forename: Masamichi
authors.initials: M
authors.lastname: Itoga
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Yuki
authors.initials: Y
authors.lastname: Moritoki
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kayaba
authors.forename: Junichi
authors.initials: J
authors.lastname: Chihara
mesh_terms: D056151:Airway Remodeling / Q000502:physiology*; D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology*; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology; D007070:Immunoglobulin A / Q000378:metabolism*; D007073:Immunoglobulin E / Q000378:metabolism*; D007074:Immunoglobulin G / Q000378:metabolism*; D007274:Injections, Intraperitoneal; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000008:administration & dosage / Q000009:adverse effects; D012737:Sex Factors
chemical_list: D018925:Chemokines; D016207:Cytokines; D012739:Gonadal Steroid Hormones; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D036341:Intercellular Signaling Peptides and Proteins; D007073:Immunoglobulin E; D010047:Ovalbumin