Animal models of allergic bronchopulmonary aspergillosis

被引:0
作者
Viswanath P. Kurup
Gabriele Grunig
机构
[1] Medical College of Wisconsin and the Research Service,Allergy
[2] V A Medical Center,Immunology Division
[3] Columbia University of Physicians and Surgeons and St. Luke's-Roosevelt Hospital,Department of Pathology
来源
Mycopathologia | 2002年 / 153卷
关键词
allergic bronchopulmonary aspergillosis; murine model; cytokines; chemokines; knockout mice; immunotherapy;
D O I
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中图分类号
学科分类号
摘要
Among the allergic fungi, Aspergillus fumigatus, a saprophytic mold, distributed widely in the environment is a frequently recognized etiologic agent in a number of allergic conditions. Among the different allergic diseases caused by this fungus, allergic bronchopulmonary aspergillosis (ABPA) is by far the most significant one. The immunopathogenesis of this disease is not fully understood. Although several immunomodulatory treatments are available for allergic disease, none of them are applicable or relevant or useful in fungal induced allergy. It is essential to understand the pathogenesis of the disease including the antigen induced immunoregulation and the resulting factors, such as cytokine, chemokines, pathways activating factors, inflammatory and airway remodeling factors need to be understood for intervening with appropriate treatment. Animal models are essential in understanding these features of the disease. Several models of allergic aspergillosis have been developed in recent years in various animals. However, murine models have been studied more carefully and extensively. The exposure to antigen in mice leads to allergy very similar to ABPA with high IgE, elevated peripheral blood and lung eosinophils, pulmonary inflammation, and airway hyperreactivity. The role of various cytokines and chemokines and their receptors were also studied. In addition, immunotherapy and vaccination have been attempted in recent years using the murine model of ABPA. This review covers the murine model of Aspergillus induced allergy and asthma and presented critically our current understanding of the subject and the potential application of such a model in future for developing treatment modalities.
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页码:165 / 177
页数:12
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共 323 条
[31]  
Bansal NK(1997)Proteases from Am J Respir Cell Mol Biol 16 674-682
[32]  
Fink JN(1978) induce release of proinflammatory cytokines and cell detachment in airway epithelial cell lines Int Arch Allergy Appl Immunol 56 325-333
[33]  
Greenberger PA.(1992)Purification and characterization of factors produced by Infect Immun 60 1952-1956
[34]  
Knutsen AP(1993) which affect human ciliated respiratory epithelium J Leukoc Biol 53 264-267
[35]  
Slavin RG.(1997)IgE and eosinophil regulation in a murine model of allergic aspergillosis Clin Immunol Immunopathol 84 216-220
[36]  
Hogaboam CM(1989)Allergeninduced bronchial hyperreactivity and eosinophilic inflammation occur in the absence of IgE in a mouse model of asthma Science 245 308-310
[37]  
Blease K(1996)Requirements for allergen-induced airway hyperreactivity in T-and B-celldeficient mice J Exp Med 183 95-201
[38]  
Mehrad B(1996)Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient nice J Clin Invest 98 2332-2345
[39]  
Steinhauser ML(2000)Allergic airway sensitization induces T cell activation but not airway hyperresponsiveness in B cell-deficient mice J Immunol 165 2603-2611
[40]  
Standiford TJ(2000)Allergen-specific IgE and IL-5 are essential for the development of airway hyperresponsiveness J Immunol 165 1564-1572