Early phase bronchoconstriction in the mouse requires allergen-specific IgG

被引:19
作者
Crosby, JR
Cieslewicz, G
Borchers, M
Hines, E
Carrigan, P
Lee, JJ
Lee, NA
机构
[1] Mayo Clin Scottsdale, Dept Biochem & Mol Biol, Div Hematol Oncol, Scottsdale, AZ 85259 USA
[2] Mayo Clin Scottsdale, Dept Biochem & Mol Biol, Div Pulm Med, Scottsdale, AZ 85259 USA
关键词
D O I
10.4049/jimmunol.168.8.4050
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Allergen provocation of allergic asthma patients is often characterized by an initial period of bronchoconstriction, or early phase reaction (EPR), that leads to maximal airway narrowing within 15-30 min, followed by a recovery period returning airway function to baseline within 1-2 h. In this study, we used a defined OVA provocation model and mice deficient for specific leukocyte populations to investigate the cellular/molecular origins of the EPR. OVA-sensitized/challenged wild-type (C57BU6J) mice displayed an EPR following OVA provocation. However, this response was absent in gene knockout animals deficient of either B or T cells. Moreover, transfer of OVA-specific IgG, but not IgE, before the OVA provocation, was capable of inducing the EPR in both strains of lymphocyte-deficient mice. Interestingly, an EPR was also observed in sensitized/challenged mast cell-deficient mice following an OVA provocation. These data show that the EPR in the mouse is an immunologically based pathophysiological response that requires allergen-specific IgG but occurs independent of mast cell activities. Thus, In the mouse the initial period of bronchoconstriction following allergen exposure may involve neither mast cells nor IgE-mediated events.
引用
收藏
页码:4050 / 4054
页数:5
相关论文
共 36 条
[21]   Cytokine and eosinophil responses in the lung, peripheral blood, and bone marrow compartments in a murine model of allergen-induced airways inflammation [J].
Ohkawara, Y ;
Lei, XF ;
Stampfli, MR ;
Marshall, JS ;
Xing, Z ;
Jordana, M .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1997, 16 (05) :510-520
[22]   Serum IgE levels, atopy, and asthma in young adults: Results from a longitudinal cohort study [J].
Peat, JK ;
Toelle, BG ;
Dermand, J ;
vandenBerg, R ;
Britton, WJ ;
Woolcock, AJ .
ALLERGY, 1996, 51 (11) :804-810
[23]   EARLY AND LATE-PHASE ASTHMATIC REACTIONS - A HYPOTHESIS [J].
PICADO, C .
ALLERGY, 1992, 47 (04) :331-333
[24]   LATE ASTHMATIC RESPONSES INDUCED BY RAGWEED POLLEN ALLERGEN [J].
ROBERTSON, DG ;
KERIGAN, AT ;
HARGREAVE, FE ;
CHALMERS, R ;
DOLOVICH, J .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1974, 54 (04) :244-254
[25]   DEVELOPMENT AND TRANSFER OF IMMEDIATE CUTANEOUS HYPERSENSITIVITY IN MICE EXPOSED TO AEROSOLIZED ANTIGEN [J].
SALOGA, J ;
RENZ, H ;
LACK, G ;
BRADLEY, KL ;
GREENSTEIN, JL ;
LARSEN, G ;
GELFAND, EW .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 91 (01) :133-140
[26]   Proinflammatory roles of T-cell receptor (TCR)γδ and TCRαβ lymphocytes in a murine model of asthma [J].
Schramm, CM ;
Puddington, L ;
Yiamouyiannis, CA ;
Lingnheld, EG ;
Whiteley, HE ;
Wolyniec, WW ;
Noonan, TC ;
Thrall, RS .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2000, 22 (02) :218-225
[27]  
Sur S, 1996, J IMMUNOL, V157, P4173
[28]   A dominant role for mast cell Fc receptors in the Arthus reaction [J].
Sylvestre, DL ;
Ravetch, JV .
IMMUNITY, 1996, 5 (04) :387-390
[29]   Development of eosinophilic airway inflammation and airway hyperresponsiveness in mast cell-deficient mice [J].
Takeda, K ;
Hamelmann, E ;
Joetham, A ;
Shultz, LD ;
Larsen, GL ;
Irvin, CG ;
Gelfand, EW .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (03) :449-454
[30]   Expression of interleukin 9 in the lungs of transgenic mice causes airway inflammation, mast cell hyperplasia, and bronchial hyperresponsiveness [J].
Temann, UA ;
Geba, GP ;
Rankin, JA ;
Flavell, RA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (07) :1307-1320