Asthma. Pathologic basis of disease Research Paper

Asthma. Pathologic basis of disease - Research Paper Example Asthma can be divided into different groups on the basis of severity of attacks that are mild intermittent, mild, moderate and severe persistent asthma. But typically the asthma is classified into extrincsic asthma and intrinsic asthma. Extrinsic asthma is set off by type 1 hypersensitivity reaction caused by an extrinsic antigen. Intrinsic asthma is initiated by various mechanisms including pulmonary infections caused by viruses especially, cold, stress, exercise and inhaled irritants. Some categories classify asthma in accordance to the agent that causes the constriction of air passages for example seasonal asthma, exercise asthma, occupational asthma, drug induced asthma and asthmatus bronchitis. The genetic susceptibility to type 1 hypersensitivity, chronic inflammation and bronchial hypersensitivity are the major factors that cause asthma. Our immune system contains Type 2 helper T cells (Th2) which is type of CD4+ helper T cell secretes interleukins. The interleukins then promote allergic inflammations and stimulate B cells to produce IgE and different antibodies. Type 1 helper T cells (Th1) are also a type of CD4+ helper T cell which secretes interferon-ÃŽ ³ (gamma) and intereukin-2. The interferon-ÃŽ ³ (gamma) and interleukin-2 activates the macrophages and cytotoxic T cells which kills the viruses and other invading organisms. These two types of helper T cells form an immunoregulatory loop that is the cytokines from type 1 helper T cells inhibit type 2 helper T cells and cytokines from type 2 helper T cells inhibit type 1 helper T cells. These two types of helper T cells respond to different immunogenic stimuli and try to destroy them. Any imbalance in the regulatory loop of these two types of helper T cells makes it easier for the viruses and agents to attack the bronchopulmonary tree and cause inflammation which leads to asthma. In patient suffering from hypersensitivity as occur in asthma, when an antigen is presented to the skin, a wheal and flare reaction occurs. This wheal and flare reaction is clear example of hypersensitivity type 1. In air passages when the allergen reaches the epithelial lining it stimulates the induction of type 2 helper T cells (Th2). The type 2 helper T cells secrete various cytokines such as interleukin 4 (IL-4) and interleukin 5 (IL-5). The interleukin 4 (IL-4) then triggers the production of immunoglobulin IgE by the B cells and promotes the growth of mast cells. The interleukin 5 promotes the growth and activation of eosinophills. The reaction mediated by IgE to the allergens elicit an acute response and late phase reaction. The acute response to the allergens consist of bronchoconstriction, edema, mucous secret ion and in rare cases the decrease of blood pressure. The acute response occurs by this mechanism; the contact of antigens to the mast cells stimulates the secretion of mediators which mediate the reaction. In the case of air passage diseases when the allergens reach the mucosal surface, the reaction of allergens first occurs with the mucosal mast cells. In this reaction mediators are secreted which opens the tight junction in between the mucosal cells and improve the entrance of the antigens to the submucosal mast cells. This reaction causes the broncoconstriction, edema and mucous secretion which is acute response. Vagal stimulation in lungs also called bronchoconstrictio