Allergic Rhinitis

Rhinitis can be induced by allergic stimuli, non-allergic triggers or both (mixed rhinitis) (Figure 1). The underlying mechanism leading to nasal symptoms thus varies depending on the type of rhinitis. Allergic rhinitis only occurs in patients with a genetic predisposition to developing allergies. Although all people are constantly exposed to environmental allergens, it is only those patients with the innate ability to become sensitized that develop symptoms. In these sensitive individuals, repeated exposure to aeroallergens causes B cell activation and maturation into plasma cells, which produce specific IgE antibodies. The IgE binds to specific receptors on the surface of basophils and mast cells. When cell bound specific IgE is cross-linked by the sensitizing allergen, the cells release or generate chemical mediators which produce the allergic symptoms. Activated mast cells release preformed histamine and generate newly synthesized leukotrienes, prostaglandins, kinins, and other compounds. The end result of this mediator release is an immediate hypersensitivity reaction with itching, sneezing, and congestion due to increased vascular permeability, vasodilatation, and increased mucus production. The vascular leakage of plasma proteins contributes to both rhinorrhea and nasal congestion.

Further release of inflammatory mediators causes a late-phase reaction that prolongs nasal symptoms after an allergen exposure. Cytokines and chemokines released and generated during this late phase reaction recruit additional inflammatory cells. These cells in turn release further inflammatory mediators which can worsen nasal symptoms and prime the nasal mucosa so that future allergen exposures lead to more rapid onset and often more severe symptoms. Up to 50% of patients with asthma have allergic rhinitis.