Immunoglobulin E or IgE is an antibody that remains in very small quantities in the body. The concentration of this antibody increases in the body when you experience an allergic attack. During an allergy attack, IgE binds itself to the allergen and causes an inflammation. Once this happens, the rest of the symptoms of the allergic reaction begin to appear.
IgE has a significant role to play in asthma. When the body is exposed to allergens, IgE becomes activated. The allergens induce T-cells that help activate B-cells. These then develop plasma cells that trigger the release of more antibodies. When allergens are inhaled into the respiratory tract, they attach themselves into the mucous membranes. This activates the immune system and releases the antibodies that can fight these allergens. Since the allergens are perceived as foreign objects by the immune system, it immediately fires up and releases the appropriate antibodies to deal with the invasion. The B-cells in the body trigger the production of IgE antibodies specific to the particular allergen. This entire process of production of the antibodies usually takes about a few weeks.
Once released, IgE antibodies attach themselves to mast cells, which are the receptors in the inflammatory cells. The rest of the unattached IgE remain free in the body and keep floating in the blood stream. When the allergen is reintroduced in the respiratory tract, the entire process occurs again, and the IgE bound on the mast cells may cross link to the new allergens. This cross linking of the IgE releases other chemicals such as histamines and prostaglandins. All of these chemical mediators further induce inflammation and the symptoms of allergy-induced asthma.
It is due to the release of these chemical mediators that symptoms such as bronchial constriction, wheezing, and coughing are triggered. With each repeated exposure and the resulting inflammation in the mucous membranes, the cells involved get inflamed and damaged. Sometimes, this damage is permanent. The airway may become permanently constricted or the volume becomes reduced, making the body more prone to experiencing asthma attacks. Some asthma patients also experience permanent scarring of the airways, which may result in other complications in both breathing and respiration.
Doctors may recommend some long-term medications that prevent the remodeling of airways as well as scarring of the lung tissues in asthma patients. Until now, the therapies and medications only reduce the symptoms and increase the body’s ability to be resilient. However, there is no treatment for the prevention of any long-term damage. These long-term medications can attack the inflammation rather aggressively so that optimal lung function can be maintained. This will also significantly reduce the risk of any permanent damage to the lungs and the rest of the respiratory system.
Since asthma is an allergic disease and there is a significant involvement of immunoglobulin E levels in the triggering of this condition, medical scientists have not been able to cure it. Fortunately, allergists and pulmonologists, along with some of other specialists have been able to study the disease and have made it treatable enough for patients to be able to live with it.
Some recent studies have shown that asthma as well as the predisposition to produce excessive levels of IgE is both inherited, and that is why asthma is considered largely a genetic and hereditary disease. Due to the close association of IgE and asthma, there is an attempt to use IgE blockers in order to find a long-term treatment and prevention for the disorder. While such medications and treatments have not yet been introduced, scientists are attempting to formulate treatments based on this principle.
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http://www.ncbi.nlm.nih.gov/pubmed/11240941Warning: The reader of this article should exercise all precautionary measures while following instructions on the home remedies from this article. Avoid using any of these products if you are allergic to it. The responsibility lies with the reader and not with the site or the writer.