Laboratory of Allergic Diseases

Allergic Inflammation Section

Description of Research Program

Allergic inflammation may lead to significant disability and even death, as occurs in over 5000 patients annually in the United States. In the majority of patients with allergic inflammatory diseases, studies have shown an aberrant polarization towards a Th2-type cytokine pattern. The major research goal of the Allergic Inflammation Section (AIS) is to understand whether allergic inflammation may be down-regulated in pre-existing Th2 conditions, and, if so, to identify the mechanisms involved. Such data could lead to new methods for immunologic intervention in asthma and other atopic diseases. The current research efforts of the Allergic Inflammation Section focus on the maintenance of tissue homeostasis by cytokine immunomodulation, and can be divided into three thematic components and projects.

Major Areas of Research

• Project I. Ascaris suum suppresses allergic inflammation through induction of immunomodulatory cytokines
• Project II. Control of eosinophil-mediated allergic inflammation through specific inhibitory receptors
• Project III. Understanding the multifaceted role of IL-21 in allergic inflammation

To study the prevention of allergic responses both systemically and in the tissue microenvironment, we employ mouse models of allergic disease. In our primary mouse model, we challenge animals via aerosolization and can assess lung inflammation by performing bronchoalveolar lavage (BAL) or through immunohistochemistry on lung samples. In addition, we can assess airway hyperresponsiveness to allergens (i.e., ragweed or cat dander) using either whole body plethysmography or tracheal cannulation. This model allows us to determine not only the inflammatory response in the lung (or lack thereof), but also how such inflammation affects the airway response.

In a secondary model, we use topical allergen challenge to induce allergic conjunctivitis. This model allows us to easily observe mast cell degranulation and mucous production, and allows for topical treatment regimens. Once we have identified genes that appear to be important in our mouse model, we are planning to collaborate with the clinical side of the laboratory to determine if the same gene dysregulation is operating in patients with asthma.

Andrea Keane-Myers, Ph.D., Section Chief
Virgilio Bundoc, D.V.M.
Brittany Wetzel, Ph.D.
Hillary Norris
Agnieszka Boesen

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