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The Rothenberg laboratory has several broad objectives that encompass the specific research hypotheses currently being investigated in the laboratory.
Regulation of Gastrointestinal Eosinophils. The major goals of this project are to analyze gastrointestinal eosinophils at baseline and during Th2-associated allergic responses in the gastrointestinal tract to determine mechanisms of their regulation during homeostasis and disease.
Mechanism of Steroid Action and Resistance in Allergic Disease. The major goal of this project is to optimize the efficacy of steroids for allergic disease by investigating the mechanisms of steroid action and resistance in allergic disease. Model systems in vitro and in vivo are employed.
Epigenetic Regulation of Allergic Disease. The major goals of this project are to elucidate gene-environment interactions in allergic disease and to define the epigenetic mechanisms that account for these interactions and their clinical and therapeutic significance.
Mechanistic Analysis of Eosinophilic Esophagitis. The major goal of this project is to understand the development of experimental eosinophilic esophagitis (EoE) in mice by exploring the mechanisms of antigen sensitization and dendritic cell involvement.
Epithelial-derived Eotaxin-3 and Eosinophilic Esophagitis. The major goal of this project is to understand the role of epithelial-derived eotaxin-3 in human eosinophilic esophagitis (EoE). Studies involve cellular distribution of eotaxin-3 and its receptor, the role and mechanisms of an eotaxin-3 single-nucleotide polymorphism in disease pathogenesis and the effect of glucocorticoid therapy on eotaxin-3 expression and esophageal transcript profiles.
IL-13 and Eosinophilic Esophagitis. The major goal of this project is to identify the expression and role of IL-13 in eliciting human eosinophilic esophagitis (EoE) and in experimental EoE in mice.
Candidate Gene Approach and Genome-wide Association Analysis for Eosinophilic Esophagitis. The major goal is to employ a candidate gene approach and genome-wide association studies (GWAS) to identify genetic risk factors for eosinophilic esophagitis (EoE) and to gain molecular insight into disease pathogenesis.
Role of CREB-binding Protein (CBP) in Eosinophilic Esophagitis. The major goal of this project is to analyze the role of CREB-binding protein (CBP) in the pathogenesis of eosinophilic esophagitis (EoE).
Role of Eotaxins and CCR3 in IL-13-induced Asthma. The major goal of this project is to define the individual and combined roles of eotaxin-1, eotaxin-2, IL-5 and CCR3 in IL-13-elicited lung responses.
Desmoglein 1 in EE - Read More.
The Role of Desmoglein 1 in Eosinophilic Esophagitis (EE)
Desmoglein1 (DSG1) is an integral component of the desmosome complex that plays a role in the structural integrity of the epithelial cell layers. Microarray data, immunofluorescence and Western blot show that DSG1 mRNA and protein are downregulated in the esophagus of EE patients. Our lab has also found a single-nucleotide polymorphism (SNP) in DSG1 that is correlated with EE disease. We are currently studying the effects of DSG1 downregulation on cell adherence with shRNA-transduced cell lines as well as how the DSG1 promoter may regulate the decrease of this protein in EE.
EE Diagnosis is Invasive - Read More.
Finding a Less Invasive Method of Diagnosing Eosinophilic Esophagitis (EE)
Currently the diagnosis of EE, and assessment of treatment response, involves invasive endoscopy and biopsy procurement and analysis and is not always accurate. Our lab is working on a more definitive molecular diagnostic test, which may also prove to be less invasive. This research involves developing a multigene panel of the genes involved in the “EE signature” into an array format that can be run using clinical samples from patients. This array should also be able to tell us which patients will be responsive to specific treatments as well as predict disease severity and quality of life for these patients.
Cadherin-like 26 in EGID – Read More
Cadherin-like 26 (CDH26) Expression and Function in eosinophilic gastrointestinal disorders (EGIDs)
The uncharacterized protein CDH26 is highly expressed in esophageal and gastric epithelial cells of patients with eosinophilic esophagitis (EE) and eosinophilic gastritis (EG), respectively, compared to the corresponding epithelial cells of normal (NL) individuals. We are investigating whether this molecule may have a role in EGID pathogenesis by overexpressing CDH26 in esophageal and gastric cell lines and monitoring their phenotypes. Additionally, we are performing biochemical characterization of this molecule to determine how it may affect cell adhesion and other cell functions.
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