This U19 Asthma and Allergic Diseases Cooperative Research Center (U19) Program brings together a team of investigators in three interactive projects and two cores to focus on the pathobiology of specific innate immune mechanisms in asthma that are dysfunctional but can be restored by novel therapies. In our proposal, we focus on the critical innate immune factors surfactant protein A (SP-A), a lipid constituent of surfactant, palmitoyl-oleoyl-phosphatidylglycerol (POPG) and Toll-like receptor interacting protein (Tollip). The investigators in this program, who have a long history of collaboration, are at two institutions, University of Arizona and National Jewish Health. The Administrative Core of this Program will perform an important role to maintain productive and vibrant collaboration, ensure and track adherence to NIH and other relevant regulations and guidelines, and manage activities that will continue to strengthen the research community surrounding this Program. The Administrative Core has the following Specific Aims: (1) Foster and maintain interaction among team members, with the Internal and External Advisory Committees, and with the NIH through communications and Program meetings, including annual Internal and External Advisors meetings and a regular seminar series; (2) Manage fiscal and other resources by working with the project and core leaders to help develop collaborations and to leverage additional resources in support of the Program's goals. (3) Track Program outputs and outcomes to ensure timely progress toward our goals, using a research timeline to ensure integration of its components and timely deliverables. This U19 program has the potential to change the approach to asthma with novel therapeutic alternatives and the Administrative Core will be the engine that facilitates these efforts.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
5U19AI125357-05
Application #
9971435
Study Section
Special Emphasis Panel (ZAI1)
Project Start
Project End
Budget Start
2020-07-01
Budget End
2021-06-30
Support Year
5
Fiscal Year
2020
Total Cost
Indirect Cost
Name
University of Arizona
Department
Type
DUNS #
806345617
City
Tucson
State
AZ
Country
United States
Zip Code
85721
Dakhama, Azzeddine; Chu, Hong Wei (2018) The Use of CRISPR-Cas9 Technology to Reveal Important Aspects of Human Airway Biology. Methods Mol Biol 1799:371-380
Ito, Yoko; Schaefer, Niccolette; Sanchez, Amelia et al. (2018) Toll-Interacting Protein, Tollip, Inhibits IL-13-Mediated Pulmonary Eosinophilic Inflammation in Mice. J Innate Immun 10:106-118
Ito, Yoko; Al Mubarak, Reem; Roberts, Nicole et al. (2018) IL-13 induces periostin and eotaxin expression in human primary alveolar epithelial cells: Comparison with paired airway epithelial cells. PLoS One 13:e0196256
Lugogo, Njira; Francisco, Dave; Addison, Kenneth J et al. (2018) Obese asthmatic patients have decreased surfactant protein A levels: Mechanisms and implications. J Allergy Clin Immunol 141:918-926.e3
Roberts, Nicole; Al Mubarak, Reem; Francisco, David et al. (2018) Comparison of paired human nasal and bronchial airway epithelial cell responses to rhinovirus infection and IL-13 treatment. Clin Transl Med 7:13
Kummarapurugu, Apparao B; Zheng, Shuo; Ledford, Julie et al. (2018) High-Mobility Group Box 1 Upregulates MUC5AC and MUC5B Expression in Primary Airway Epithelial Cells. Am J Respir Cell Mol Biol 58:126-128
Noutsios, George T; Willis, Amanda L; Ledford, Julie G et al. (2017) Novel role of surfactant protein A in bacterial sinusitis. Int Forum Allergy Rhinol 7:897-903
Carr, Tara F; Kraft, Monica (2017) Management of Severe Asthma before Referral to the Severe Asthma Specialist. J Allergy Clin Immunol Pract 5:877-886
Jiang, Di; Matsuda, Jennifer; Berman, Reena et al. (2017) A novel mouse model of conditional IRAK-M deficiency in myeloid cells: application in lung Pseudomonas aeruginosa infection. Innate Immun 23:206-215
Huang, C; Jiang, D; Francisco, D et al. (2016) Tollip SNP rs5743899 modulates human airway epithelial responses to rhinovirus infection. Clin Exp Allergy 46:1549-1563