Anaphylaxis-FloridaGulfCoastUniversity.pptVIP

Anaphylaxis IgE Mediated Hypersensitivity What is anaphylaxis? An acute systemic allergic reaction The result of a re-exposure to an antigen that elicits an IgE mediated response Usually caused by a common environmental protein that is not intrinsically harmful Often caused by medications, foods, and insect stings It is a Type I hypersensitivity History 1st recorded 2640BC in hieroglyphics bee sting of a pharoah Richet Portier South Seas Man-o-war coined term anaphylaxis IgE Binds irreversible to FcεRI receptors on mast cells, basophils, and eosinophils Is usually for parasitic infections E heavy chain Mast Cell Has high affinity for IgE molecules (105 IgE/cell) Originates in the bone marrow, reside in connective tissues Increases host response to parasitic infections Contain immunological mediators in granules ie. Histamine, ECF-A, HMW-NCF 2 populations that vary in granule content and activity Connective tissue Mucosal IgE FcRI Receptor Symptoms Peripheral vasodilation vascular permeablility (edema) Bronchospasm Cardiac arrhythmias Smooth muscle contractions Sensitization Antigen is presented by antigen presenting cells TH2 cells induce B cell activation CD40 ligand and cytokines B cells undergo isotype switching and produce antibody Serum antibody is bound by the mast cells The allergic response Secondary presentation of antigen produces an immediate response controlled by mast cells Granule contents are released Cell mediated response proceeds Sensitization Response What is happening? Initial exposure sensitizes mast cells. Antigen specific IgE molecules attach to high affinity Fc receptors on the mast cell surface. Cross linking of IgE molecules on surface causes intracellular signaling pathway Inflammatory mediators are released upon degranulation Mediators Involved Include histamine, proteases, chemotactic factors, leukotrienes, prostaglandin D, and cytokines Primary: released before degranulation Interleukin 4 used by T cells induces B cell mat