Asthma is type one hypersensitivity reaction. It could be atopic (extrinsic) or non-atopic (intrinsic). In atopic asthma:
In early phase, When asthmatic people inhale allergen, this will lead to bronchoconstriction due to the release of mediators by mast cells (histamine, prostaglandin, and leukotrienes) and this will lead to contraction of airway smooth muscle. When the person Expose to an allergen the IgE antibodies level will increase. The change in IgE production is related to Th2 (these cells are not normally found in the lung, they also promote inflammation and increase humoral immunity by promoting antibodies production). IgE antibodies bind to receptors on mast cells. So when an allergen is inhaled and is in contact with mast cells, the release of …show more content…
IL-4 is responsible for stimulating IgE production, IL-5 will produce eosinophil in the bone marrow then release them into circulation and IL-13 will stimulate mucus production. Also epithelial cell will produce chemokines that will promote Th2 cells. In addition, there is direct stimulation for the parasympethatic system by vagal receptors and this will lead to bronchoconstriction.
The late phase response (after 4-8 hours) includes monocytes, DC and neutrophils, also T lymphocytes, eosinophils, and basophils. The release of mediators by these cells will cause contraction. Goblet cells will produce more mucus that will plug the airway and cause hyper-responsiveness, which will exacerbate the symptoms.
- Eosinophil is the most common cell that accumulates in asthma. They are activated by chemokines (eotaxin). Eosinophils will produce mediators that cause contraction of smooth muscle and toxic products (major basic protein, eosinophil peroxidase and eosinophil cationic protein) that will damage epithelial cells in the airway. It will also produce cytokines (e.g interleukins) that cause remodeling and fibrosis for the
In early phase, When asthmatic people inhale allergen, this will lead to bronchoconstriction due to the release of mediators by mast cells (histamine, prostaglandin, and leukotrienes) and this will lead to contraction of airway smooth muscle. When the person Expose to an allergen the IgE antibodies level will increase. The change in IgE production is related to Th2 (these cells are not normally found in the lung, they also promote inflammation and increase humoral immunity by promoting antibodies production). IgE antibodies bind to receptors on mast cells. So when an allergen is inhaled and is in contact with mast cells, the release of …show more content…
IL-4 is responsible for stimulating IgE production, IL-5 will produce eosinophil in the bone marrow then release them into circulation and IL-13 will stimulate mucus production. Also epithelial cell will produce chemokines that will promote Th2 cells. In addition, there is direct stimulation for the parasympethatic system by vagal receptors and this will lead to bronchoconstriction.
The late phase response (after 4-8 hours) includes monocytes, DC and neutrophils, also T lymphocytes, eosinophils, and basophils. The release of mediators by these cells will cause contraction. Goblet cells will produce more mucus that will plug the airway and cause hyper-responsiveness, which will exacerbate the symptoms.
- Eosinophil is the most common cell that accumulates in asthma. They are activated by chemokines (eotaxin). Eosinophils will produce mediators that cause contraction of smooth muscle and toxic products (major basic protein, eosinophil peroxidase and eosinophil cationic protein) that will damage epithelial cells in the airway. It will also produce cytokines (e.g interleukins) that cause remodeling and fibrosis for the