Inflammation that is induced by allergens is a common characteristic in both allergic rhinitis and asthma that the 4 year old patient has been diagnosed with. The 4-year old had previous exposure to allergens, thus making his airways sensitive to allergens. Later exposures to the allergen caused the inflammatory response that involved the Immunoglobin E (IgE), with symptoms being characteristic of allergic rhinitis or asthma. IgE is involved in allergic responses caused by chronic exposure of the airways to allergens (Siraganian, 2003). IgE-mediated immune responses lead to early allergic reactions. The process involves the binding of Immunoglobin E to the FceRI receptor cells that are situated on the surfaces of basophils and mast cells. These receptors are considered to be high-affinity receptors for IgE. The complex of the IgE and the FceRI cross-links with an allergen of a multivalent nature to cause a release in the mediators of inflammation (Siraganian, 2003). This implies that basophils and mast cells must express the FceRI receptors for the IgE-mediated allergic reactions to occur, as the binding site for the IgE is found on the α-subunit of the FceRI receptors. It should be noted that the mere binding of the IgE to the FceRI receptors cannot lead to the activation of the basophils and the mast cells, or their degranulation. Instead, the process of cross-linking involves the receptor-bound IgE with a multivalent antigen must occur. The process of receptor aggregation follows. The process of cross-linking is said to lead to a quick phyosphorylation of the ITAMs of B and Y subunits of the receptor (Siraganian, 2003).
The binding of the IgE on the surfaces of the mast and basophil cells results in the activation of the cells and the release of mediators of inflammation, some of which were already partially formed in the mast cells and basophils. Some of the mediators include histamine and chemotactic factors. The IgE-triggered mechanism also leads to the formation of inflammatory mediators from precursor molecules. One such compound is the platelet-activating factor. The mediators cause an up regulation of leukocyte-endothelial adhesion molecules. The expression of the FceRI on the surface of the cells is upregulated markedly once the IgE comes into contact with the mast cells and basophils (Siraganian, 2003). It is, therefore, common to have high levels of IgE in the serum and hyper-responsiveness of the airway in IgE related asthma or allergic rhinitis. Cytokines such as the Interleukin 4, 6, and 13, and TNF-alpha are also expressed further after the IgE-FceRI complex formation (Satoshi et al., 2010). Resultantly, the sensitivity of the respiratory and upper airways to the allergen increases and the production of cytokines increases. The release of these molecules in the respiratory and upper airways causes mucosal engorgement, followed by fluid exudation. Edema is also present. The fluid accumulates in the airways, leading to airway constriction. The mediators also stimulate the afferent nerve endings, thereby causing nasopharyngeal pruritus, as well as sneezing (Arshad & Holgate, 2001).
Once inflammation occurs in the respiratory and upper airways, the vessels dilate markedly, while they also become more permeable and prone to leak the mucus that is secreted. Moreover, the secretion of mucus increases. Moreover, the acute symptoms seen in allergic rhinitis and asthma are as a result of the action of the inflammatory mediators on the nerves, vessels, and tissues of the airways (Siraganian, 2003). The wheezing experienced in both conditions is a reflex reaction to irritation and an attempt to clear the congested and constricted airways.