by Mark Lin

Created on: February 12, 2009

Asthma, the condition which is usually closely associated with allergy in a vast majority of allergy reactions, has two variants, one associated with allergy and the other unrelated. The variant of asthma related to allergy is known as extrinsic asthma, characterized by genetic inheritance, atopy, and local proliferation of inflammatory cells.

Extrinsic asthma is genetically inherited, thus the onset begins very early in childhood. Since the cause takes root in the defective genes, one may infer that the defect is avoidable only by eliminating the offending agent from the presence of the environments without the administration of immunosuppressant therapy.

Atopy, the secretion of IgE, is the most distinguishing characteristic that sets it apart from its other variant, intrinsic asthma. The pathomechanism of intrinsic asthma occurs in the following way, and may be divided into two phases, the first being the vascular phase and the second the inflammatory phase.

As an individual is exposed to an allergen, the antigen of the offending agent is presented to the CD4+ T cell by APC, resulting in the production of interleukin-5 by the former. CD4+ T cell is also known as the T helper cell, and may be regarded as the conductor of all immune reactions. The chemokine activates eosinophils, which in turn secretes IgE. As regarded by the general population, eosinophils are thought of as the causative cells in allergic reactions, but as one may see below, the reality opposes the common believe. IgE activates mast cells and basophils, which secretes the ultimate offending substance found in asthma, histamine. Thus, the group of cells that may be held responsible for allergic reactions and ultimately asthma are the basophils and mast cells. The aim in the prevention of the disease state is aimed at the inhibition of histamine release rather than hindering the production of IgE. Histamine is a very potent vasodilator that causes the redness and warmth observed in allergic reactions. Furthermore, it also serves as a bronchoconstriction, resulting in the characteristic bronchoconstriction observed in asthma. The pathomechanism of extrinsic asthma is as discussed above.

Asides from histamine's effect in increasing the vascular permeability, the chemokine's abilities in triggering inflammatory reactions should not be overlooked. At the site of release, the inflammatory reaction takes place approximately 8 hours after the initial release. Histamine stimulates the metabolism of arachidonic acid into its various products, such as leukotrienes, thromboxane, etc., that induce further inflammation. To conclude, the inflammatory importance of histamine lies mostly in its ability to put the metabolism of arachidonic acid in motion.

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