Pathophysiology

Exposure to potential allergens (e.g. grass pollen, animal dander) in susceptible individuals leads to the formation of allergen-specific immunoglobulin E (IgE) antibodies that bind to the surface of mast cells. On subsequent exposure, the specific allergen interacts with the IgE on the mast cells resulting in the release of chemical mediators including histamine, leukotrienes and prostaglandins. These cause immediate nasal itching, sneezing, vascular dilatation and glandular secretion experienced as congestion and rhinorrhoea.

A late phase reaction follows several hours later, mediated by eosinophils and other inflammatory cells. This results in persistence of characteristic symptoms – sneezing, rhinorrhoea, nasal itching and obstruction. Upper airway inflammation provokes bronchial hyper-reactivity, so cough, wheezing and shortness of breath can also be present. In addition, neuro-immune mechanisms are thought to contribute to the immune-inflammatory process.

Allergens are foreign proteins (e.g. the proteins at the heart of a pollen grain, in animal saliva present on animal hair and fur, in the faecal pellets of house dust mites and cockroaches, and found in nuts or grains). Metals (e.g. nickel, chromium) and acrylates (e.g. in dental fillings or gel nails) can become immunogenic when they act as haptens and bind to endogenous proteins. It is the protein-hapten complex that elicits the immunological response.