Immunopathologic responses to Aspergillus antigen in interleukin-4 knockout mice

被引:30
作者
Kurup, VP
Guo, J
Murali, PS
Choi, H
Fink, JN
机构
[1] Vet Affairs Med Ctr, Res Serv 151I, Milwaukee, WI 53295 USA
[2] Vet Affairs Med Ctr, Lab Serv, Milwaukee, WI 53295 USA
[3] Med Coll Wisconsin, Dept Med, Allergy & Immunol Div, Milwaukee, WI 53226 USA
[4] Med Coll Wisconsin, Dept Pathol, Milwaukee, WI 53226 USA
来源
JOURNAL OF LABORATORY AND CLINICAL MEDICINE | 1997年 / 130卷 / 06期
关键词
D O I
10.1016/S0022-2143(97)90106-2
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Two strains of interleukin-4 (IL-4) gene knockout mice were studied and compared with wild strains to determine the role of IL-4 in the immunopathogenesis of murine allergic aspergillosis. Animals immunized intraperitoneally were subsequently challenged with Aspergillus antigen intranasally. The animals were evaluated for total serum immunogolulin E (IgE) levels, Aspergillus-specific IgG antibody isotypes, peripheral blood eosinophils, cytokine and chemokine mRNA transcripts in spleen cells, and pulmonary histology. No serum IgE was detected in animals deficient in the IL-4 gene. Aspergillus-specific IgG(1) was detected in all animals, while enhanced revels of IgG(2a) were detected in IL-4 knockout animals challenged with A. fumigatus antigen. There were no differences in the peripheral blood or lung eosinophils in the two groups of mice exposed to A. fumigatus. These results indicate that lung injury in Aspergillus-antigen challenged animals may be the result of the eosinophil mediators and that IgE-mediated injury may not be significant in this model, which may be a significant variation between the model and human allergic aspergillosis.
引用
收藏
页码:567 / 575
页数:9
相关论文
共 35 条
[1]   CELLULAR EVENTS IN THE BRONCHI IN MILD ASTHMA AND AFTER BRONCHIAL PROVOCATION [J].
BEASLEY, R ;
ROCHE, WR ;
ROBERTS, JA ;
HOLGATE, ST .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1989, 139 (03) :806-817
[2]  
BOCHNER BS, 1994, ANNU REV IMMUNOL, V12, P295
[3]   EOSINOPHILIC INFLAMMATION IN ASTHMA [J].
BOUSQUET, J ;
CHANEZ, P ;
LACOSTE, JY ;
BARNEON, G ;
GHAVANIAN, N ;
ENANDER, I ;
VENGE, P ;
AHLSTEDT, S ;
SIMONYLAFONTAINE, J ;
GODARD, P ;
MICHEL, FB .
NEW ENGLAND JOURNAL OF MEDICINE, 1990, 323 (15) :1033-1039
[4]   ASSOCIATION OF ASTHMA WITH SERUM IGE LEVELS AND SKIN-TEST REACTIVITY TO ALLERGENS [J].
BURROWS, B ;
MARTINEZ, FD ;
HALONEN, M ;
BARBEE, RA ;
CLINE, MG .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 320 (05) :271-277
[5]   MECHANISMS OF PERSISTENT AIRWAY INFLAMMATION IN ASTHMA - A ROLE FOR T-CELLS AND T-CELL PRODUCTS [J].
BUSSE, WW ;
COFFMAN, RL ;
GELFAND, EW ;
KAY, AB ;
ROSENWASSER, LJ .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1995, 152 (01) :388-393
[6]   SINGLE-STEP METHOD OF RNA ISOLATION BY ACID GUANIDINIUM THIOCYANATE PHENOL CHLOROFORM EXTRACTION [J].
CHOMCZYNSKI, P ;
SACCHI, N .
ANALYTICAL BIOCHEMISTRY, 1987, 162 (01) :156-159
[7]  
DEMONCHY JGR, 1985, AM REV RESPIR DIS, V131, P373
[8]   QUANTITATIVE LOCUS ANALYSIS OF AIRWAY HYPERRESPONSIVENESS IN A/J AND C57BL/6J MICE [J].
DESANCTIS, GT ;
MERCHANT, M ;
BEIER, DR ;
DREDGE, RD ;
GROBHOLZ, JK ;
MARTIN, TR ;
LANDER, ES ;
DRAZEN, JM .
NATURE GENETICS, 1995, 11 (02) :150-154
[9]   Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model [J].
Foster, PS ;
Hogan, SP ;
Ramsay, AJ ;
Matthaei, KI ;
Young, IG .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (01) :195-201
[10]  
GALLI SJ, 1993, NEW ENGL J MED, V328, P257