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The BCG Polysaccharide and Nucleic Acid Preparation (bacillus Calmette Guerin-polysaccharide nucleic acid (BCG-PSN)) is an immune regulatory medicine mainly used for the prevention and treatment of chronic bronchitis, flu (cold) and asthma. The mechanism of the product is to mediate and regulate the cellular immunity of the patient. It increases the bodies own mechanisms to defend itself from external pathogenic challenge. The major pathways and mechanisms are as follows; Pathway Allergic reactions in chronic bronchitis, flu (cold) and asthma are triggered when allergens cross-link preformed IgE bound to the high-affinity receptor FCe RI on mast cells as well as on basophils and eosinophils all able to interact with each other, and which can also drive IgE production. All three cell types express Fce RI, although eosinophils only express it when activated. When these specialised granulocytes are activated, they express cell-surface CD40L and secrete IL-4; like TH2 cells therefore, they can drive class switching and IgE production by B cells. The interaction between these specialised granulocytes and B cells can occur at the site of the allergic reaction, as B cells are observed to form germinal centers at inflammatory foci. The immediate allergic reaction is followed by a more sustained inflammation, known as the late-phase response. This late response involves the recruitment of other effector cells, notably TH2 lymphocytes, eosinophils and basophils, which contribute significantly to the immunopathology of an allergic response. The vaccine stabilizes the mast cells, reduces degranulation and leads to improved overall condition of the patient. Mast cells Mast cells line the body surfaces and serve to alert the immune system to local infection. They contain granules rich in acid molecules. Degranulation occurs within seconds after activation (by antigen cross linking Fce RI-bound IgE), releasing a variety of preformed mediators. Among these are histamine- a short lived vasoactive amine that causes an immediate increase in local blood flow and vessel permeability-and the enzymes mast-cell chymase, tryptase, and serine esterases. The latter might in turn activate matrix metalloproteinases, which collectively break down tissue matrix proteins. Tumor necrosis factor (TNF)-a is also stored in mast-tissue cell granules and is released in large amounts form both preformed and newly synthesized pools on mast-cell activation. It causes endothelial activation with upregulation of the expression of adhesion molecules, which promotes the influx of inflammatory leukocytes and lymphocytes. The inflammatory response is further sustained by synthesis of chemokines, lipid mediators such as leukotrienes and platelet activating factor, as well as of further cytokines such as IL-4. Finally, when re-exposure to allergen triggers an allergic reaction, the effects are focused on the site at which mast-cell degranulation occurs. Late allergic response The late phase reaction is caused by the induced synthesis and release of mediators including leukotrienes, chemokines and cytokines from the activated mast cells. These recruit other leukocytes, including eosinophils and TH2 lymphocytes, to the site of inflammation. If antigen persists and stimulates allergen-specific TH2 cells, which in turn promote eosinophilia and further IgE production. This late response can easily convert into a chronic inflammatory response being quite often an important cause of much serious long-term illness as for example chronic asthma caused by mast-cell degranulation.
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