title: Physiologic assessment of allergic rhinitis in mice: role of the high-affinity IgE receptor (FcepsilonRI).
abstract: BACKGROUND
  There have been few reports using animal models to study the development of allergic rhinitis. Characterization of such a model in mice would be advantageous given the availability of reagents and gene-manipulated strains.
  
  
  OBJECTIVE
  We sought to develop a murine model of allergic rhinitis in the absence of lower airway changes.
  
  
  METHODS
  After sensitization and challenge, both wild-type and FcepsilonRI-deficient mice were studied for their ability to develop early- and late-phase nasal responses. In the invasive approach, direct measurements of nasal airway resistance (R(NA)) were obtained; in the noninvasive approach using whole-body plethysmography, respiratory frequency and expiratory and inspiratory times were monitored. In both approaches, nasal responses were determined either acutely after challenge (early phase) or 24 hours after challenge (late phase).
  
  
  RESULTS
  After challenge of sensitized mice, R(NA) significantly increased. In parallel, respiratory frequency significantly decreased and was highly correlated with the increases in R(NA). Sensitized wild-type mice had an early-phase nasal response and persistent nasal blockage (late-phase response) after allergen challenge. In contrast, sensitized and challenged FcepsilonRI alpha-chain-deficient mice did not have an early-phase nasal reaction and exhibited reduced nasal blockage and lower IL-13 levels in nasal tissue homogenates.
  
  
  CONCLUSIONS
  These data indicate that FcepsilonRI is essential to development of an early-phase nasal response and contributes to the development of the late-phase nasal response. These invasive and noninvasive approaches provide new opportunities to evaluate the mechanisms underlying the development of nasal responses to allergen and to assess various therapeutic interventions.
authors.affiliation: Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA.
authors.forename: Satoko
authors.initials: S
authors.lastname: Miyahara
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Miyahara
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Takeda
authors.forename: Anthony
authors.initials: A
authors.lastname: Joetham
authors.forename: Erwin W
authors.initials: EW
authors.lastname: Gelfand
mesh_terms: D000281:Administration, Intranasal; D000403:Airway Resistance; D000818:Animals; D001667:Binding, Competitive; D004334:Drug Administration Schedule; D004804:Eosinophils / Q000473:pathology; D007114:Immunization; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood; D007274:Injections, Intraperitoneal; D018793:Interleukin-13 / Q000378:metabolism; D007700:Kinetics; D051379:Mice; D018345:Mice, Knockout; D009296:Nasal Cavity / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D017455:Receptors, IgE / Q000172:deficiency / Q000378:metabolism*; D015656:Respiratory Mechanics; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*
chemical_list: D007074:Immunoglobulin G; D018793:Interleukin-13; D017455:Receptors, IgE; D007073:Immunoglobulin E; D010047:Ovalbumin