The """"""""Asthma Clinical Core B"""""""" will be a resource to provide well characterized subjects and specimens from cohorts of asthma and control subjects (bronchial brushings, BAL, endobronchial biopsy, sputum, blood, lung tissue) that will be used in each of the three projects comprising this AADCRC (Broide, Project 1;Croft, Project 2;Zuraw, Project 3). These specimens will allow investigators in the AADCRC to determine whether the inflammatory and remodeling pathways they are studying are differentially regulated in asthma compared to a control population. In addition to the cross sectional cohorts of asthma and control subjects. Core B will also provide specimens (sputum, blood, BAL, bronchial brushings, endobronchial biopsy) from well characterized asthmatic subjects obtained before and after allergen challenge, as well as before and after rhinoviral challenge. Overall, the provision of these specimens from asthma and control subjects will allow the individual projects to determine whether defined inflammatory and remodeling pathways are different in asthma compared to control subjects, as well as determine whether these inflammatory and remodeling pathways are regulated to be expressed by two common precipitants of asthma namely allergen and virus.

Public Health Relevance

Inhalation of airborne allergens such as cat and dust mite or respiratory viruses may result in damage and scarring of the bronchial tubes in susceptible asthmatics. This project will provide increased understanding of the cause of this scarring and suggest potential ways to identify asthmatics at risk for developing scarring of their lungs, or potential new treatments.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
2U19AI070535-06
Application #
8195762
Study Section
Special Emphasis Panel (ZAI1-PA-I (M1))
Project Start
2011-09-01
Project End
2016-08-31
Budget Start
2011-09-01
Budget End
2012-08-31
Support Year
6
Fiscal Year
2011
Total Cost
$328,145
Indirect Cost
Name
University of California San Diego
Department
Type
DUNS #
804355790
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Doherty, Taylor A; Broide, David H (2017) Pathways to limit group 2 innate lymphoid cell activation. J Allergy Clin Immunol 139:1465-1467
Chen, Jun; Miller, Marina; Unno, Hirotoshi et al. (2017) Orosomucoid-like 3 (ORMDL3) upregulates airway smooth muscle proliferation, contraction, and Ca2+ oscillations in asthma. J Allergy Clin Immunol :
Lund, Sean J; Portillo, Alex; Cavagnero, Kellen et al. (2017) Leukotriene C4 Potentiates IL-33-Induced Group 2 Innate Lymphoid Cell Activation and Lung Inflammation. J Immunol 199:1096-1104
Cavagnero, Kellen; Doherty, Taylor A (2017) Cytokine and Lipid Mediator Regulation of Group 2 Innate Lymphoid Cells (ILC2s) in Human Allergic Airway Disease. J Cytokine Biol 2:
Song, Dae Jin; Miller, Marina; Beppu, Andrew et al. (2017) Rhinovirus Infection of ORMDL3 Transgenic Mice Is Associated with Reduced Rhinovirus Viral Load and Airway Inflammation. J Immunol 199:2215-2224
Miller, Marina; Tam, Arvin B; Mueller, James L et al. (2017) Cutting Edge: Targeting Epithelial ORMDL3 Increases, Rather than Reduces, Airway Responsiveness and Is Associated with Increased Sphingosine-1-Phosphate. J Immunol 198:3017-3022
Eastman, Jacqueline J; Cavagnero, Kellen J; Deconde, Adam S et al. (2017) Group 2 innate lymphoid cells are recruited to the nasal mucosa in patients with aspirin-exacerbated respiratory disease. J Allergy Clin Immunol 140:101-108.e3
Miller, Marina; Rosenthal, Peter; Beppu, Andrew et al. (2017) Oroscomucoid like protein 3 (ORMDL3) transgenic mice have reduced levels of sphingolipids including sphingosine-1-phosphate and ceramide. J Allergy Clin Immunol 139:1373-1376.e4
Croft, Michael; Siegel, Richard M (2017) Beyond TNF: TNF superfamily cytokines as targets for the treatment of rheumatic diseases. Nat Rev Rheumatol 13:217-233
Mehta, Amit K; Duan, Wei; Doerner, Astrid M et al. (2016) Rhinovirus infection interferes with induction of tolerance to aeroantigens through OX40 ligand, thymic stromal lymphopoietin, and IL-33. J Allergy Clin Immunol 137:278-288.e6

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