Abstract

Allergic diseases continue to pose a significant public health burden in modernized societies. Although the etiology of allergic diseases is unknown, they are thought to develop as a result of aberrant Th2 immune responses in genetically susceptible individuals. Despite this recognition, the factors driving Th2-mediated immune responses have remained elusive. Our preliminary data suggests the novel paradigm that allergen exposure induces epithelial cell injury which results in the release of an epithelial-derived factor, trefoil factor 2. Tff2, in turn induces the release of the

Public Health Relevance

Although allergic diseases have long posed a significant public health burden, the factors predisposing some individuals to the development of these disorders are unknown. Herein, we will test the novel hypothesis that dysregulation of the production of an epithelial-derived factor. Trefoil factor 2, drives susceptibility to allergic disorders through a pathway involving the

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
5U19AI070235-08
Application #
8707647
Study Section
Special Emphasis Panel (ZAI1-PA-I (M1))
Project Start
Project End
Budget Start
2013-09-01
Budget End
2014-08-31
Support Year
8
Fiscal Year
2013
Total Cost
$384,306
Indirect Cost

  Institution

Name
Cincinnati Children's Hospital Medical Center
Department
Type
DUNS #
071284913
City
Cincinnati
State
OH
Country
United States
Zip Code
45229

  Publications

O'Shea, Kelly M; Aceves, Seema S; Dellon, Evan S et al. (2018) Pathophysiology of Eosinophilic Esophagitis. Gastroenterology 154:333-345
Ghandikota, Sudhir; Hershey, Gurjit K Khurana; Mersha, Tesfaye B (2018) GENEASE: real time bioinformatics tool for multi-omics and disease ontology exploration, analysis and visualization. Bioinformatics 34:3160-3168
Rosenberg, C E; Mingler, M K; Caldwell, J M et al. (2018) Esophageal IgG4 levels correlate with histopathologic and transcriptomic features in eosinophilic esophagitis. Allergy 73:1892-1901
Martin, Lisa J; He, Hua; Collins, Margaret H et al. (2018) Eosinophilic esophagitis (EoE) genetic susceptibility is mediated by synergistic interactions between EoE-specific and general atopic disease loci. J Allergy Clin Immunol 141:1690-1698
Gour, Naina; Lajoie, Stephane; Smole, Ursula et al. (2018) Dysregulated invertebrate tropomyosin-dectin-1 interaction confers susceptibility to allergic diseases. Sci Immunol 3:
Perez Ramirez, Leilanie; Wendroth, Heepke; Martin, Lisa J et al. (2018) High number of early respiratory infections in association with allergic sensitization to mold promotes childhood asthma. J Allergy Clin Immunol 141:1921-1924.e4
Herr, Andrew B (2018) Evolution of an allosteric ""off switch"" in apoptotic caspases. J Biol Chem 293:5462-5463
Johansson, Elisabet; Hershey, Gurjit K Khurana (2018) Contribution of an impaired epithelial barrier to the atopic march. Ann Allergy Asthma Immunol 120:118-119
Lynch, Mary K; Barnes, Margaux J; Dimmitt, Reed A et al. (2018) Disease-Related Predictors of Health-Related Quality of Life in Youth With Eosinophilic Esophagitis. J Pediatr Psychol 43:464-471
Khoury, Paneez; Akuthota, Praveen; Ackerman, Steven J et al. (2018) Revisiting the NIH Taskforce on the Research needs of Eosinophil-Associated Diseases (RE-TREAD). J Leukoc Biol 104:69-83

Showing the most recent 10 out of 112 publications