Asthma is known as a chronic inflammation disorder of the airways and can be divided as atopic and non-atopic. “Atopic asthma also known as extrinsic asthma is triggered by the environment.” (Barnes, 1996) Atopic asthma is the most common form of asthma. Atopic asthma causes inflammation and is mediated by systemic IgE production. Non-atopic asthma is considered intrinsic asthma which is less common. Non-atopic asthma is inflammation and or constriction of the airways that is not caused by exposure to an allergen. “In fact, inflammation is mediated by local IgE production.” (Barnes, 1996) “Intrinsic asthma known as exercise-induced asthma, plus the chemical induced asthma is very tough to treat.” (Barnes, 1996) Intrinsic asthma is usually
…show more content…
During this reaction, the allergen will be engulfed by dendrite cells and activate them. Columnar epithelial cells will be able to recognize that activation and secrete a substance called thymic stromal lymphocytes. Thymic stromal lymphocytes will condition activated dendritic cells to produce chemokines in order to attract specifically T helper 2 cells to the …show more content…
“T helper 2 cells job is to promote humeral immunity from stimulating plasma cells through interleukin 13 and interleukin 4.” (Barnes, 1996) The following process will promote IgE antibody production by the plasma cells. IgE cells will bind with mast cells to create the IgE mast cell complex. T helper 2 cells itself through interleukin 9, will stimulate mast cell activity. Another thing T helper 2 cells will do is promote eosinophil production from bone marrow through interleukin 5 to the lungs. The inhaled allergen will bind to IgE mast cell complex which causes the mast cell to release histamine, prostaglandins and leukotrienes. All this histamine will stimulate smooth muscle in the airways to cause constriction also known as bronchoconstricition. An endothelial cell will then release stem cell factors that will eventually, maintain mast cells to the area. “During all this process or memory of IgE will repeat itself every time there is an inhaled allergen trigger.” (Barnes,
During this reaction, the allergen will be engulfed by dendrite cells and activate them. Columnar epithelial cells will be able to recognize that activation and secrete a substance called thymic stromal lymphocytes. Thymic stromal lymphocytes will condition activated dendritic cells to produce chemokines in order to attract specifically T helper 2 cells to the …show more content…
“T helper 2 cells job is to promote humeral immunity from stimulating plasma cells through interleukin 13 and interleukin 4.” (Barnes, 1996) The following process will promote IgE antibody production by the plasma cells. IgE cells will bind with mast cells to create the IgE mast cell complex. T helper 2 cells itself through interleukin 9, will stimulate mast cell activity. Another thing T helper 2 cells will do is promote eosinophil production from bone marrow through interleukin 5 to the lungs. The inhaled allergen will bind to IgE mast cell complex which causes the mast cell to release histamine, prostaglandins and leukotrienes. All this histamine will stimulate smooth muscle in the airways to cause constriction also known as bronchoconstricition. An endothelial cell will then release stem cell factors that will eventually, maintain mast cells to the area. “During all this process or memory of IgE will repeat itself every time there is an inhaled allergen trigger.” (Barnes,