Research Grant Awardees

AAFA Research Grant Awardees

For more than 25 years, AAFA has helped scientists find new treatments for asthma and allergies. We are proud to support research and hope it will help us find a cure.


2015-2016 Sheldon C. Siegel – AAFA Investigator Grant Award

Hongmei ZhangHongmei Zhang, PhD, University of Memphis

Does Epigenetic Methylation Explain the Gender-Switch In Adolescent Asthma?

Early prevention of asthma is essential to reduce the burden of this high-impact and avoidable disease. Asthma is more common in boys among pre-teenagers, but during adolescence it becomes more common in girls.  This “switch-over” is likely caused by factors that influence gene activities, e.g., DNA methylation of nucleotides. DNA methylation does not alter genes but is a process of putting some (strong or weaker) chemical marks on the nucleotides. The strength of the marks can be changed and consequently will make genes less or more expressed (and thus influence the risk of asthma). In our study, we will 1) assess genome-wide DNA methylation of specific nucleotides called CpG sites using blood samples taken before and after adolescent transition; for each gender we will identify specific DNA methylation that is associated with asthma status change during adolescent transition; 2) test the association of DNA methylation with asthma risk factors (growth changes, use of contraceptives and pain killers, and smoking); this assessment will identify asthma risk factors that influence DNA methylation.

     Our overall hypothesis: the reversal of asthma prevalence in adolescence can be explained by the introduction of methylation differences between genders during the pre- to post-adolescent transition. The findings from the projects have strong potential to critically impact our ability to prevent incidence and promote remission of asthma during adolescence.


2014-2015 Sheldon C. Siegel – AAFA Investigator Grant Award

Vikas AnathyVikas Anathy, PhD, University of Vermont

Endoplasmic Reticulum Stress Signaling in Allergen-Induced Airway Remodeling

The lung is exposed to many potential allergens, toxins, particulates and pathogens. Repeated exposure to these insults can trigger a vicious cycle of repair and remodeling of the lung ultimately leading to stiffness of the lungs and respiratory failure. We have discovered that repeated allergen exposure in the lung trigger a stress response in a specialized structure inside the lung cells called the endoplasmic reticulum (ER). The stress is called as ER stress. The ER stress subsequently leads to killing of lung cells and ultimately resulting in lung stiffness. We will address this problem using genetically modified mouse to understand the disease process and pharmacological inhibitors to block the activity of specific proteins to alleviate the disease process. Thus, the current proposal will investigate how allergen induced ER stress is involved in initiating scarring of the lung. The outcome of this research will help us better understand the process of allergen initiated lung injury and to identify novel therapeutic targets to alleviate the process of lung stiffening.


2013-2014 AAFA Fellowship – New Faculty Award

Caroline SokolCaroline Sokol, MD, PhD, Harvard University

Allergen Recognition and Th2-type Immune Activation

Why do allergens, which are harmless environmental substances, trigger immune responses that lead to asthma and allergies? In order to answer this, we have developed a mouse model of allergy in which we track the earliest interactions between allergens and the immune system. Using this model, we have identified the existence of a cell necessary for the initiation of the allergic response and have shown that blocking migration of this cell prevents the allergic response.  We are now working to identify this cell and how it promotes allergy, with the ultimate goal of identifying new therapeutic targets to treat allergic diseases.



2013-2014 Sheldon C. Siegel – AAFA Investigator Grant Award

Cherie SingerCherie Singer, PhD, University of Nevada

Integrin-Based Therapies for the Treatment of Asthma

Traditional asthma therapy has relied on drugs that alleviate inflammation and shortness of breath. However, neither of these treatments targets the function of muscle lining the airways, which is responsible for bringing air into the lungs. These muscle cells expand and divide during asthma to contribute to symptoms and are linked together by proteins known as integrins. Integrins act as molecular glue, interacting with other proteins to keep muscle cells attached and allowing them to communicate with their surroundings. This study will examine the impact of one of these integrins, known as 7 integrin, to asthma development in a genetically-modified mouse that expresses 7 integrin in the airways and identify compounds targeting 7 integrin function in search of new therapies for asthma. 



2012-2013 AAFA Fellowship – New Faculty Award

Suzanne CasselSuzanne Cassel, MD, University of Iowa

Determining the Cell Type on Which Tim-1 Is Required to Regulate Development of T-Cell Responses

Asthma and allergies are the manifestation of an inappropriate immune response to an innocuous environmental protein. Unfortunately, these disorders are increasing in frequency and are associated with significant morbidity and mortality. Many theories have been developed and investigated to determine the mechanism by which the detrimental immune response develops. Genetic analyses have revealed a link between the development of asthma and a specific part of a chromosome; studies in mice have confirmed the equivalent chromosomal section is associated with a predisposition to asthma. One gene in that region that seems particularly important is T-cell immunoglobulin domain and mucin domain-1 (Tim-1). Many different immune cells express this protein on their surface, but how it influences the development of allergies is not known.  We study mice that have a specific deletion in Tim-1 and compare their ability to develop allergies to mice that express Tim-1 normally. Our findings suggest Tim-1 plays an important role in down-regulating asthmatic responses as mice that do not have Tim-1 have more severe allergic airway disease. We plan to define the mechanism by which Tim-1 influences the development of allergies so it can be exploited to treat or even prevent asthma and allergies in patients.


2011-2012 Sheldon C. Siegel – AAFA Investigator Grant Award

Steven F. Ziegler, PhDSteven Ziegler, PhD, Benaroya Research Institute

TSLP, RSV and Airway Inflammation






2011-2012 Sheldon C. Siegel – AAFA Investigator Grant Award

Pedro C Avila, MDPedro Avila, MD, Northwestern University Feinberg School of Medicine

 Dendritic Cells in Asthma Exacerbations







2011-2012 Sheldon C. Siegel – AAFA Investigator Grant Award

Magdalena Gorska Magdalena Gorska, MD, PhD, Allergy and Clinical Immunology Division, National Jewish Health

 The Importance of the Signaling Protein Unc119 in Th2 Responses in Asthma

Allergic asthma is orchestrated by cytokines. Cytokines are secretory molecules that serve as means of communication between cells in inflammation. Some cytokines e.g. interleukin 4 (IL-4) promote allergy while others e.g. interferon γ (IFNγ) suppress it. The mechanisms that regulate release of IL-4 and IFNγ from cells are not understood. Dr. Gorska has discovered that these two cytokines are released through separate routes. The IL-4 route is unconventional and involves intracellular structures called endosomes. Dr. Gorska has also identified molecules that control the endosomal secretion of IL-4. Dr. Gorska’s research identifies fundamental mechanisms of asthma and may pave the way for development of novel treatments for asthma.



2010-2012 Sheldon C. Siegel – AAFA Investigator Grant Award

Gilman B. Allen, MD, University of Vermont and State Agriculture College          

Reflux and Asthma: The Mechanisms of Acid-Induced Airways Hyper-Responsiveness






2009-2010 Sheldon C. Siegel – AAFA Investigator Grant Award

Robert Freishtat, MD, MPH, Children’s National Medical Center, Washington, D.C.  

Genes and Environmental Tobacco Smoke

African American inner-city children have five times the national rate of asthma than other populations in the United States. This disparity can be attributed only in part to social risk factors inherent in inner-city living and poverty. A large portion of the remaining disparity is likely explained by interactions between genes and environmental factors. In a genetic study of inner-city pediatric asthma, a team of investigators from Children’s National Medical Center in Washington, D.C. proposes to develop a statistical model that identifies the contribution of environmental tobacco smoke exposure to a child’s asthma severity.