Pathophysiology of perennial allergic rhinitis

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Abstract
Allergic rhinitis involves an early phase, largely mediated through mast cells, and a late phase which involves cellular infiltration and mediator release. In the early phase, mast cells release mediators as a result of antigen cross‐linking adjacent immunoglobulin E molecules bound to mast cell surfaces. This results in an accumulation of histamine which gives rise to the characteristic symptoms of rhinitis ‐ sneezing, itching, rhinorrhoea and congestion. The late phase of the allergic response (hours after challenge) involves infiltration of the nasal epithelium by eosinophils, basophils, monocytes and T‐lymphocytes, which release leukotrienes, kinins, histamine and a host of other mediators. The most important part of the late‐phase response is probably mediated via the production of cytokines (IL‐4, IL‐5, IL‐6, IL‐8, GM‐CSF and RANTES) by mast cells, Th2 lymphocytes or epithelial cells. The infiltration of tissues by cells normally present only in the blood is brought about by the production of adhesion molecules, such as VCAM‐1 and E‐selectin, which cause circulating eosinophils, basophils and T‐lymphocytes to adhere to endothelial cells before moving through the endothelium into the tissue (diapedesis). Neuronal reflexes also play a role in the allergic response, both by mediating local responses to mediators and possibly playing a part in the activation of T‐lymphocytes. The allergic response has also been shown to be less intense in a hot, humid environment, and more marked in a cold, dry environment, possibly due to changes in osmolality of the nasal surface fluid. Similar factors may play a role in the actiology of non‐allergic rhinitis.