Immunoglobulin E (IgE) plays a significant function in allergic infections such as asthma. IgE is an antibody. It is also vital to mention that it is present in small amounts in the human body. It usually binds itself to allergens. As a result, it is in a position to agitate the production of inflammatory substances from mast cells. Hence, a series of allergic reactions may be initiated when IgE attaches itself to cells in the mast (Lipps, 2009). The most commonly affected cells are those of the respiratory system and the upper airways.
When an individual who is already suffering from an allergic disease is exposed to an allergen in a repeated manner, he or she may easily react against it. In other words, the respiratory and upper airways cells react to the allergens. Second, B cells are activated by the T cells during the T cell reaction. As a result, additional antibodies are released by the developed plasma cells after the T cell reaction. The immune nature of IgE explains why it is an instrumental part of the entire defense system of the human body. In the case of type I hypersensitivity, IgE has also been found to be an essential ingredient. The component also serves a crucial function in most allergic conditions,
In regards to the effects on respiratory cells and upper airways, it is pertinent to mention that the allergic cascade is the main effect of igE on the respiratory cells and the upper airways. Once an allergic person is exposed to allergen, the defense system of the body begins to experience a cascade of reactions. The initial reaction may not b very severe. However, subsequent reactions are extremely severe. A particular pattern is followed by an allergic reaction. To begin with, the respiratory cells and the upper airways are sensitized by an allergen. The latter is followed by some form of an early phase response. Eventually, the affected region experiences a late-phase response.
Ciliated epithelium plays the role of lining up the respiratory tract. Other crucial parts that assist the ciliated epithelium in its role are the respiratory bronchioles and nasal ostia. Nonetheless, reduction in the amount of air that flows through the air passage is contributed by various physiological mechanisms. For example, vascular mucosa engorgement is the main cause of obstruction that occurs in the upper airway. On the other hand, the larger part in the lung is bronchoconstriction. This type of reduction in size is caused by the encircling smooth muscle. At this point, it is vital to mention that the upper airways do not host the encircling smooth muscle.
However, the airways located in the upper and lower regions play well coordinated roles and as such, none can work in the absence of the other. As a matter of fact, when the nasal mucosa is stimulated, it may occasion major changes in the responsive nature of the bronchioles.
In most instances, patients are diagnosed with hyper responsiveness. In addition, it has been documented that the trigeminal afferent nerves are remarkably affected by receptor simulation that takes place sinuses and the nasal regions. The cascading consequence is also observed in the parasympathetic fibers due to the degree of stimulation that takes place. However, the vagus nerve acts as the launch pad for the entire process. Eventually, all the previously mentioned processes interfere with the bronchomotor tone.
It is also necessary to describe the pathophysiology of how the symptoms of sneezing, mucous production, and airway constriction occur especially in regards to IgE. Asthma is one of the infections that cause inflammatory pathogenesis. The inflammatory reactions usually involve cellular participants and pathogenic events. In most cases, the bronchial mucosa and nasal mucosa are the main symptoms when the airway is constricted. The inflammation of airway passage and the upper respiratory system has a number of consequences. The same consequences can also be perceived as symptoms associated with sneezing, mucous production and airway constriction.
For instance, patients diagnosed with asthma may experience airway hyper-responsiveness, abnormal secretion of mucous, edema of swelling of regions close to the inflammation, leakage, vascular permeability, and increased vasodilation.
Nonetheless, the lungs and nose experience a difference in terms of the physiologic and structural makeup (Porth & Matfin, 2009). It is the latter that usually aggravates or cause the specific symptoms of the disease when the allergic reactions have already taken place. When the lower and upper airways are exposed among atopic individuals, the concerned allergen may be readily sensitized. Thereafter, an inflammatory response that is complex (2-phased) might be generated when the airway mucosa is exposed.
It might equally be prudent to mention that different types of chemicals are usually released during the preceding phases. One of the most dominant chemicals released is eosinophils. As a result, the inflammatory reaction is intensified, prolonged and sustained. Some of the additional chemicals that intensify inflammation include leukotrienes cytokine and cationic proteins. The most prominent symptoms during the last phase include airway congestion or constriction and increased production of mucous (Acton, 2013).
Acton, Q.A. (2013). Immunoglobulin Isotypes—Advances in Research and Application. Atlanta: Scholarly Editions.
Lipps, B.V. (2009). Immunoglobulin E (Ige): Novel Treatment for Lowering the Concentration of Ige. Pittsburgh: Rose Dog Books.
Porth, C. & Matfin, G. (2009). Pathophysiology: Concepts of altered health states. Philadelphia, PA: Lippincott Williams & Wilkins.