Grants

E•A•T  is solely focused on funding research.  We do not fund other food allergy related initiatives such as educational programming, publications, advocacy related efforts, operations for treatment centers, etc.   While these are extremely important initiatives, we believe other organizations do them very well.  

Goal is to accelerate research

Our goal is to accelerate the most promising ideas in food allergy research toward the clinical testing and expansion of shorter-term treatments and longer term solutions involved in the root causes, triggers, and processes of food allergy progression.  

Objective funding process

Our medical advisory board is comprised of highly knowledgeable scientists and physicians who are leaders in the field but not conducting their own studies.  

 

On May 23, 2016 EAT announced it is funding the following studies:

 

Biomarkers

Molecular Gene Expression During Allergic Reactions to Food: Identifying Signatures Which Correlate with Severity of Reaction’

Jonathan M. Spergel, MD, PhD, Division of Allergy-Immunology, The Children’s Hospital of Philadelphia, Perelman School of Medicine at University of Pennsylvania

Paul J. Turner, FRACP PhD, Section of Pediatrics (Allergy-Immunology), Faculty of Medicine, Imperial College London, United Kingdom.

More Information

Microbiome

‘Characterization of Prebiotic Dietary Fibers to Prevent or Treat Food Allergy’

Cathryn R. Nagler, PhD, Bunning Food Allergy Professor, Professor of Pathology, Medicine, Pediatrics and The College, The University of Chicago

More Information

Oral Immunotherapy 

‘Improving Safety for the Food Allergy-Asthma Syndrome’

Sharon Chinthrajah, MD, Kari Nadeau, MD, PhD, Pulmonary and Critical Care Medicine, Allergy and Immunology, Sean N Parker Center for Allergy and Asthma Research, Stanford University 

More Information

 

Study Summaries

‘Molecular Gene Expression During Allergic Reactions to Food: Identifying Signatures Which Correlate with Severity of Reaction’

Jonathan M. Spergel, MD, PhD, Division of Allergy-Immunology, The Children’s Hospital of Philadelphia, Perelman School of Medicine at University of Pennsylvania

Paul J. Turner, FRACP PhD, Section of Pediatrics (Allergy-Immunology), Faculty of Medicine, Imperial College London, United Kingdom.

The biggest challenge in managing individuals with food allergy is our current inability to reliably identify those people who are at risk of severe, life-threatening reaction. Our knowledge regarding the mechanisms of food allergic reactions in man is limited, partly due to the fact that animal models are of very limited relevance. We cannot explain why one person will develop life-threatening anaphylaxis to under 1/70 of a peanut, while another will develop only localized itching after eating 3-4 peanuts. Allergy tests (skin prick test size, specific IgE antibody to either a total allergen or allergen component) do not predict the severity or the sensitivity of an individual.  For example, a patient with small skin test can have life-threatening allergic reaction, while another patient with a large skin test may have a mild reaction limited to the skin. 

Understanding the mechanisms, and in particular the differences between severe and non-severe allergic reactions, is key to improving patient care. In this research we will take advantage of blood samples from a unique cohort of peanut-allergic patients that have undergone carefully-controlled food challenges to peanut under varying conditions and experienced different types of reactions.  We will use advanced molecular techniques (microarray gene expression CHIP assay) to study expression of genes which are activated during allergic reactions and then result in the release of mediators which cause the reaction. We will analyze these results to identify how the different gene expression signals are associated with the symptoms experienced by patients.   The goal is to identify molecular signatures that correlate with patterns of symptoms allowing us to predict who  is at risk for a severe reaction. 

 

‘Characterization of Prebiotic Dietary Fibers to Prevent or Treat Food Allergy’

Cathryn R. Nagler, PhD, Bunning Food Allergy Professor, Professor of Pathology, Medicine, Pediatrics and The College, The University of Chicago

Immunoregulatory responses induced by commensal bacteria are critical to preventing intestinal inflammation. Whether the intestinal microbiota also plays a role in regulating non responsiveness to the other major luminal constituent – food – has been poorly understood. Murine models developed in our laboratory demonstrate that sensitization to a food allergen is enhanced in mice that have been treated by neonatal antibiotic administration (Abx) or are devoid of commensal microbes (germ free). By selectively colonizing germ free mice we showed that the allergy-protective capacity is contained within the Clostridia, a class of anaerobic spore forming Firmicutes that resides in close proximity to the intestinal epithelium. Reintroduction of a Clostridia-containing microbiota to Abx-treated mice blocks sensitization to a food allergen. Microarray analysis of intestinal epithelial cells isolated from gnotobiotic mice identified a novel innate mechanism by which Clostridia protect against sensitization to dietary antigens. Clostridia colonization induces the production of the barrier protective cytokine IL-22 by both innate lymphoid cells and T cells in the intestinal lamina propria. IL-22-mediated effector functions, including the production of mucus and anti-microbial peptides, collectively contribute to protection against sensitization by reducing the access of dietary antigen to the systemic circulation. Our mouse model work is supported by translational studies comparing the fecal microbiota of healthy infants to that of infants with cow’s milk allergy (CMA). We find that the CMA infant microbiome has the diverse community structure typical of adults. Treatment of CMA infants with a tolerance inducing formula supplemented with the probiotic Lactobacillus rhamnosus GG (LGG) is associated with changes in microbial community structure that include the expansion of butyrate-producing Clostridia and significantly higher levels of butyrate detectable in feces. Butyrate, but not other short chain fatty acids, regulates epithelial barrier function in our mouse model. Commensal bacteria produce butyrate by fermentation of insoluble dietary fiber and we also find that mice weaned onto high fiber diets exhibit reduced intestinal permeability to food antigens. Identification of dietary fibers, and their metabolites, which regulate the intestinal epithelial barrier has great promise for the development of novel microbiome modulating approaches to prevent or treat allergic sensitization to food.

 

‘Improving Safety for the Food Allergy-Asthma Syndrome’

Sharon Chinthrajah, MD, Kari Nadeau, MD, PhD, Pulmonary and Critical Care Medicine, Allergy and Immunology, Sean N Parker Center for Allergy and Asthma Research, Stanford University 

Oral immunotherapy (OIT) is an emerging investigational therapy for food allergy. With multiple small exploratory trials and some large randomized-controlled phase 2 trials recently published, there is clear progress and interest toward making this a treatment option for patients suffering from food allergies. Understanding who is at risk for more severe reactions during OIT, the immunological mechanisms underlying the increased risk, and how to make OIT a safer process would help to make this therapy more widely available.

In patients with food allergy, asthma is a risk factor for a life threatening reaction.1,2 Interestingly, both diseases have overlapping immune mechanisms leading to “allergic inflammation” characterized by eosinophils, allergic antibodies, such as IgE, and T helper cells (Th2 cells). Though T cells are understood to be central mediators of both asthma and food allergy separately, little is known about the contribution of different T cell subsets to a combined food allergy-asthma syndrome. Recently, we have shown that omalizumab, an anti-IgE antibody extensively studied in asthma, can also be used in conjunction with OIT to desensitize patients to their food allergies in a safe and expedient manner, compared to OIT alone.4

We will to understand distinct food allergic phenotypes and determine the relative contributions of T cell subsets in these different groups and how this contributes to the safety of OIT in patients undergoing OIT with and without Omalizumab. Results from these studies will improve our understanding of the interaction between food allergy and asthma, and lead to the understanding of how omalizumab may increase safety and symptoms of these diseases during oral immunotherapy.

 

Interested grant applicants should please contact us at Research@EndAllergiesTogether.com