title: House dust mite facilitates ovalbumin-specific allergic sensitization and airway inflammation.
abstract: BACKGROUND
  Mouse models of allergic airway disease have greatly contributed to our understanding of disease induction and pathogenesis. Although these models typically investigate responses to a single antigen or allergen, humans are frequently exposed to a myriad of allergens, each with distinct antigenic potential.
  
  
  OBJECTIVE
  Given that airway exposure to ovalbumin (OVA), a prototypic innocuous antigen, induces inhalation tolerance, we wished to investigate how this response would be altered if OVA were encountered concurrently with a house dust mite extract (HDM), which we have recently shown is capable of eliciting a robust allergic airway inflammatory response that is mediated, at least in part, by granulocyte-macrophage colony-stimulating factor.
  
  
  METHODS
  Balb/c mice were exposed daily to HDM (intranasally) followed immediately by exposure to aerosolized OVA for 5 weeks. To allow the inflammatory response elicited by HDM to subside fully, mice were then allowed to rest, unexposed, for 8 weeks, at which time they were rechallenged with aerosolized OVA for 3 consecutive days.
  
  
  RESULTS
  At this time, we observed a robust eosinophilic inflammatory response in the lung that was associated with an increase in bronchial hyperreactivity. Moreover, we documented significantly elevated serum levels of OVA-specific IgE and IgG(1) and increased production of the Th2 cytokines interleukin 4 (IL-4), IL-5, and IL-13 by splenocytes stimulated in vitro with OVA.
  
  
  CONCLUSIONS
  Our data demonstrate the potential of a potent allergen such as HDM to establish a lung microenvironment that fosters the development of allergic sensitization to otherwise weak or innocuous antigens, such as OVA.
authors.affiliation: Division of Respiratory Diseases and Allergy, Center for Gene Therapeutics, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Ramzi
authors.initials: R
authors.lastname: Fattouh
authors.forename: Mahmoud A
authors.initials: MA
authors.lastname: Pouladi
authors.forename: David
authors.initials: D
authors.lastname: Alvarez
authors.forename: Jill R
authors.initials: JR
authors.lastname: Johnson
authors.forename: Tina D
authors.initials: TD
authors.lastname: Walker
authors.forename: Susanna
authors.initials: S
authors.lastname: Goncharova
authors.forename: Mark D
authors.initials: MD
authors.lastname: Inman
authors.forename: Manel
authors.initials: M
authors.lastname: Jordana
mesh_terms: D000818:Animals; D016535:Bronchial Hyperreactivity / Q000276:immunology*; D016207:Cytokines / Q000276:immunology; D005260:Female; D007073:Immunoglobulin E / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D066298:In Vitro Techniques; D007249:Inflammation / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000009:adverse effects* / Q000276:immunology; D039981:Pyroglyphidae
chemical_list: D016207:Cytokines; D007074:Immunoglobulin G; D007073:Immunoglobulin E; D010047:Ovalbumin