TY - JOUR
T1 - Physiologic assessment of allergic rhinitis in mice
T2 - Role of the high-affinity IgE receptor (FcεRI)
AU - Miyahara, Satoko
AU - Miyahara, Nobuaki
AU - Takeda, Katsuyuki
AU - Joetham, Anthony
AU - Gelfand, Erwin W.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2005/11
Y1 - 2005/11
N2 - 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 FcεRI-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 (RNA) 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, RNA 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 FcεRI α-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 FcεRI 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.
AB - 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 FcεRI-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 (RNA) 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, RNA 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 FcεRI α-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 FcεRI 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.
KW - Allergy
KW - Hyperresponsiveness
KW - Rhinitis
KW - Rodent
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U2 - 10.1016/j.jaci.2005.08.020
DO - 10.1016/j.jaci.2005.08.020
M3 - Article
C2 - 16275370
AN - SCOPUS:27644575887
SN - 0091-6749
VL - 116
SP - 1020
EP - 1027
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 5
ER -