and specific aims): Asthma is characterized pathologically by airways inflammation and physiologically by airways obstruction and hyperresponsiveness. The cellular infiltrate in asthma is pleomorphic, and includes T lymphocytes, eosinophils and mast cells. The mechanism of eosinophil recruitment and the development of airways hyperresponsiveness remain to be fully established. This application proposes to study the regulation of chemokine expression and the role of T cells, eosinophils and humoral responses in a murine model of allergic asthma.
The specific aims are: 1) To determine if antigen-specific T cell lines and clones can induce eotaxin production by endothelial and epithelial cell lines in vitro. 2) To determine the effect of anti-T cell and anti-cytokine interventions in vivo, on the expression of eosinophil-specific chemokines. 3) To determine the effect of neutralizing eotaxin in vivo, on antigen-induced pulmonary eosinophilia and airways hyperresponsiveness in a murine model of antigen-induced pulmonary eosinophilia. 4) To differentiate the respective roles of humoral vs. T cell-mediated responses on the expression of eosinophil-specific chemokines, pulmonary eosinophilia and airways hyperresponsiveness in a murine model of antigen-induced pulmonary eosinophilia.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
5R29AI041129-02
Application #
2672969
Study Section
Lung Biology and Pathology Study Section (LBPA)
Project Start
1997-09-30
Project End
2002-08-31
Budget Start
1998-09-01
Budget End
1999-08-31
Support Year
2
Fiscal Year
1998
Total Cost
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
City
Boston
State
MA
Country
United States
Zip Code
02199