The central objective of this Center application is to understand the contribution of innate immunity to allergic asthma and, in addition to the use of human subjects, it will depend heavily on an experimental model of asthma developed by Dr. David Corry. Through this focus, the intent of this proposal is to define novel endogenous and exogenous mediators of allergic inflammation that potentially contribute to the expression of allergic asthma. In defining the importance of such innate inflammatory mediators, the broad, long-term objective of this proposal is to define new means for the prevention and therapy of allergic asthma and other allergic disorders. For each of the three projects comprising this application, the experimental asthma model is required for completion of the specific aims. The Animal Core B will provide services and expertise essential to participating investigators regarding their studies in mice and cells and tissues derived from mice. The expertise of the core is focused on the in vivo model of allergic lung inflammation and the performance of immunological assays relevant to the asthma model. Objectives and responsibilities of the Core: Core B will provide participating investigators with the expertise required for establishing the allergic lung inflammation model. It will further provide assistance, essential reagents and equipment for performance of physiological and immunological assays relevant to the allergy model. Core B leader, Dr. Corry, will review all data derived from studies conducted as part of the Core and ensure uniform, high quality and appropriate interpretation of data. The specific methods supported by Core B are: 1. Establishment of an animal model of asthma. 2. Physiological evaluation of airway hyperresponsiveness. 3. Detailed immunological anaysis of bronchoalveolar lavage fluid, cells and tissues of mice. 4. Collection, storage and distribution of mouse tissue and fluid samples.
| Millien, Valentine Ongeri; Lu, Wen; Mak, Garbo et al. (2014) Airway fibrinogenolysis and the initiation of allergic inflammation. Ann Am Thorac Soc 11 Suppl 5:S277-83 |
| Knight, John M; Lee, Seung-Hyo; Roberts, Luz et al. (2014) CD11a polymorphisms regulate TH2 cell homing and TH2-related disease. J Allergy Clin Immunol 133:189-97.e1-8 |
| Porter, Paul C; Lim, Dae Jun; Maskatia, Zahida Khan et al. (2014) Airway surface mycosis in chronic TH2-associated airway disease. J Allergy Clin Immunol 134:325-31 |
| Mak, Garbo; Porter, Paul C; Bandi, Venkata et al. (2013) Tracheobronchial mycosis in a retrospective case-series study of five status asthmaticus patients. Clin Immunol 146:77-83 |
| Millien, Valentine Ongeri; Lu, Wen; Shaw, Joanne et al. (2013) Cleavage of fibrinogen by proteinases elicits allergic responses through Toll-like receptor 4. Science 341:792-6 |
| Shearer, William T; Corry, David B (2012) High prevalence of asthma in HIV-infected adults: new insights. J Allergy Clin Immunol 129:715-6 |
| Yang, Tianshu; Ramocki, Melissa B; Neul, Jeffrey L et al. (2012) Overexpression of methyl-CpG binding protein 2 impairs T(H)1 responses. Sci Transl Med 4:163ra158 |
| Grünig, Gabriele; Corry, David B; Reibman, Joan et al. (2012) Interleukin 13 and the evolution of asthma therapy. Am J Clin Exp Immunol 1:20-27 |
| Porter, Paul; Polikepahad, Sumanth; Qian, Yuping et al. (2011) Respiratory tract allergic disease and atopy: experimental evidence for a fungal infectious etiology. Med Mycol 49 Suppl 1:S158-63 |
| Porter, Paul C; Yang, Tianshu; Luong, Amber et al. (2011) Proteinases as molecular adjuvants in allergic airway disease. Biochim Biophys Acta 1810:1059-65 |
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