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Allergy and Immunology

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Research Highlights

Date
Topic
2009
February
A Pathway for Connecting Intestinal Inflammation with Metabolic Problems is Identified
2008
December
An Allergy Associated Mediator is Shown to Induce Intestinal Inflammation 
September
The Mechanism of Mast Cell Growth and Involvement in Hypereosinophilic Syndrome is Defined. 
August
A New Approach to Blocking Eosinophils in Vivo is Shown in a Pre-Clinical Study. 
July
A New Pathway Involved in Eosinophilic Esophagitis is Identified. 
July
A Novel Regulatory Molecule PIR-B in Eosinophil Activation and Inhibition is Reported.
June
The Familial Form of Eosinophilic Esophagitis is Described and the Clinical and Genetic Aspects Defined. 
June
The Action of Anti-IL-5 in Eosinophilic Patients is Defined. 
May
The Receptor Involved in Eliciting Allergic Lung Responses to IL-4 and IL-13 is Elucidated. 
March
Anti-IL-5 Therapy in Patients with Hypereosinophilia is Shown to be Successful. 
January
The Mechanism of Esophageal Scarring in Eosinophilic Esophagitis is Identified. 
2007
December
The Key Role of IL-13 in Eosinophilic Esophagitis is Identified. 
March
A Long Term Follow Up of Eosinophilic Esophagitis Patients is Reported. 
2006
November
Early Biomarkers for Eosinophilic Esophagitis are Identified.
October The Key Importance of the Eotaxin Receptor CCR3 is Reported. 
August The First Placebo Controlled Trial in Eosinophilic Esophagitis Reports Benefit of Swallowed Fluticasone. 
May
An In-Vivo Model of Hypereosinophilic Syndrome Involving FIP1L1-PDGFR is Reported. 
February Gene Discovery Linked to Mysterious Chronic Food Allergy: Study offers first molecular insight into eosinophilic esophagitis.
2004
September Two Studies in Science Point to New Evidence in Asthma Development: Eosinophils Have a Key Role in Asthma.
August
Study In The New England Journal of Medicine Indentifies Rapidly Rising Disorder.
January
Study Identifies Breakthrough Treatment For Devastating Blood Disorders.
2001
March Study Identifies Culprits in Food Allergy Inflammation.
2000
December 
Cincinnati Children's Researcher Uncovers Allergy / Reflux Link: Study Has Significant Treatment Implications.
June 
Cincinnati Children's Researchers Uncover Critical Food Allergy Pathway.

Development of Atopy and Asthma

A main focus of the research programs in the Division of Allergy and Immunology is to identify the molecules and genes, which have a role in the development of atopy and asthma, and to dissect the mechanisms by which the genes lead to the disease phenotype.

Atopic disorders, including asthma and allergic rhinitis, are very prevalent in the general population.  In a recent report on the surveillance for asthma by the National Center for Health Statistics, the authors found that asthma prevalence rates and asthma death rates are increasing nationally.  Although it is clear that both genetic and environmental influences play a role in the development of these common disorders, very little is known about the molecular mechanisms which underlie the development of allergic inflammatory conditions.

Asthma and other atopic conditions have their origins in early life.  If children can be identified early in the course of their disease or even prior to onset of the disease through genetic markers, it is possible that environmental interventions or aggressive medical therapy may delay the onset or prevent the progression of the disease process.

Clinical Research

There are several clinical research programs underway in the Division of Allergy and Immunology. These include trial of anti-cytokine therapeutics (e.g. humanized anti-human IL-5 for eosinophilic esphagitis), and phase II-IV studies.  In addition, we have a major translational research program focused on allergic diseases aimed to elucidate genetic-environmental interactions for the development of atopy and the molecular mechanisms for eosinophil-associated mucosal inflammation.

The Division of Allergy and Immunology research program focuses on defining the molecular basis underlying the development and exacerbation of diseases including asthma, food allergy and eosinophilic gastrointestinal diseases, and hypereosinophilic syndrome (chronic eosinophilic leukemia). The group has developed an array of innovative experimental animal (murine) models of allergic diseases to define the contribution of cytokines, receptors, chemokines, inflammatory cells including eosinophils, CD4+ T-cells and mast cells in the pathophysiological manifestations of allergic diseases. For example, Dr. Simon Hogan’s laboratory recently reported a novel mouse model of oral antigen hypersensitivity allowing him to define an essential role for mast cells and the cytokine interleukin-9 in gastrointestinal allergy. (Forbes, E. E. et al. IL-9- and mast cell-mediated intestinal permeability predisposes to oral antigen hypersensitivity. J. Exp. Med. 31 March 2008 [doi:10.1084/jem.20071046])

How to Reach Us

For more information about the Division of Allergy and Immunology at Cincinnati Children's Research Foundation, please call 513-803-0257, or send an e-mail to AllergyResearch@cchmc.org.