Asthma

Asthma

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     Asthma is a chronic illness that affects many people. Asthma affects approximately 155 million people around the world. The pharmaceutical industry approximates $5.5 billion in sales for asthma medication per year for a condition that is incurable.

     Asthma is an inflammatory disease of the airways. The narrowing of airways occurs due to inflammation and excessive mucous secretion. The constriction of the airway gives rise to common asthmatic symptoms of wheezing, coughing, tightness in the chest, and shortness of breath. The usual form of control for asthma is bronchiodilators and corticosteriods.

     Although, bronchiodilators are used in asthma therapy they have no effect on the inflammatory process. Bronchiodilators are a class of drug that relaxes airway smooth muscle by increasing cAMP and opening potassium channels. Corticosteriods on the other hand are now considered the first line of treatment for patients with severe and chronic asthma. Corticosteriods bind to a receptor in the cytosol, which translocates to the nucleus and binds DNA to activate genes. The main action of corticosteriods is to suppress multiple inflammatory genes, such as cytokines, inflammatory enzymes and adhesion molecules. The effectiveness of the corticosteriod is in most part due to the inhibition of transcription factors, such as AP-1 (activation protein 1), Nuclear factor-b (NF-b), and nuclear factor of activated T-cells (NF-AT), which are required for inflammatory response.

     The FcRI is the receptor for the IgE antibody. The FcRI is composed of a  chain that binds the Fc portion of the IgE, the  chain and the  chain together form a tetrameric structure. Due to the fact that release of mediators from mast cells in asthma is IgE-E dependent one approach would be to block the activation of IgE using blocking antibodies that do not result in mast cells. A humanized murine monoclonal antibody directed to the FcRI-binding domain of human IgE (rhuMAb-E25) reduces allergen specific IgE after intravenous administration. RhuMAb reduces early and late responses to inhaled allergen and eosinophils counts from induced sputum.

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Although reduction in early response to allergen, which is due to mast cells bound to IgE the reduction in late response and sputum eosinophils is unexpected, but it could be explained by blocking the effect of IgE on low affinity IgE receptors such as CD23 on antigen presenting cells (APC). Anti-IgE in mice inhibits IL-4,5 secretion and pulmonary eosinophilia by blocking Th2-cell activation in response to allergen, and this is mimicked by anti-CD23 antibody. Clinical trials for rhuMAb-E25 are now in progress.

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