Cigarette Smoke-induced Airway Hyperresponsiveness Is Not Dependent on Elevated Immunoglobulin and Eosinophilic Inflammation in a Mouse Model of Allergic Airway Disease

2002 ◽  
Vol 165 (10) ◽  
pp. 1410-1418 ◽  
Author(s):  
Edward G. Barrett ◽  
Julie A. Wilder ◽  
Thomas H. March ◽  
Teresa Espindola ◽  
David E. Bice
Keyword(s):  
Mouse Model ◽  
Cigarette Smoke ◽  
Airway Hyperresponsiveness ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Eosinophilic Inflammation

scholarly journals The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e74730 ◽  
Author(s):  
Rebecca A. Martin ◽  
Jennifer L. Ather ◽  
Rebecca Daggett ◽  
Laura Hoyt ◽  
John F. Alcorn ◽  
...  
Keyword(s):  
Adoptive Transfer ◽  
Airway Hyperresponsiveness ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Th17 Response

Eotaxin/CCL11 is involved in acute, but not chronic, allergic airway responses toAspergillus fumigatus

2002 ◽  
Vol 283 (1) ◽  
pp. L198-L204 ◽  
Author(s):  
Jane M. Schuh ◽  
Kate Blease ◽  
Steven L. Kunkel ◽  
Cory M. Hogaboam
Keyword(s):  
T Cell ◽  
Airway Hyperresponsiveness ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Th2 Cells ◽  
Wild Type ◽  
Cell Recruitment ◽  
Chronic Model ◽  
Airway Responses

Eotaxin/CCL11 is a major chemoattractant for eosinophils and Th2 cells. As such, it represents an attractive target in the treatment of allergic disease. The present study addresses the role of eotaxin/CCL11 during acute and chronic allergic airway responses to the fungus Aspergillus fumigatus. Mice lacking the eotaxin gene (Eo−/−) and wild-type mice (Eo+/+) were sensitized to A. fumigatus and received either an intratracheal challenge with soluble A. fumigatusantigens (acute model) or an intratracheal challenge with live A. fumigatus spores or conidia (chronic model). Airway hyperresponsiveness and eosinophil, but not T cell, recruitment were significantly decreased at 24 h after the soluble allergen in A. fumigatus-sensitized Eo−/− mice compared with similarly sensitized Eo+/+ mice. In contrast, the development of chronic allergic airway disease due to A. fumigatus conidia was not altered by the lack of eotaxin. Together, these data suggest that eotaxin initiates allergic airway disease due to A. fumigatus, but this chemokine did not appear to contribute to the maintenance of A. fumigatus-induced allergic airway disease.

Vitamin D3 deficiency enhances allergen-induced lymphocyte responses in a mouse model of allergic airway disease

2012 ◽  
Vol 23 (1) ◽  
pp. 83-87 ◽  
Author(s):  
Shelley Gorman ◽  
Daryl H. W. Tan ◽  
Misty J. M. Lambert ◽  
Naomi M. Scott ◽  
Melinda A. Judge ◽  
...  
Keyword(s):  
Mouse Model ◽  
Vitamin D3 ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Lymphocyte Responses ◽  
Vitamin D3 Deficiency

scholarly journals Transforming Growth Factor-β1 Suppresses Airway Hyperresponsiveness in Allergic Airway Disease

2007 ◽  
Vol 176 (10) ◽  
pp. 974-982 ◽  
Author(s):  
John F. Alcorn ◽  
Lisa M. Rinaldi ◽  
Elizabeth F. Jaffe ◽  
Mirjam van Loon ◽  
Jason H. T. Bates ◽  
...  
Keyword(s):  
Growth Factor ◽  
Airway Hyperresponsiveness ◽  
Transforming Growth Factor ◽  
Airway Disease ◽  
Transforming Growth Factor Β1 ◽  
Allergic Airway Disease
Sign in / Sign up

Export Citation Format

Share Document