PATHOPHYSIOLOGY OF PERENNIAL ALLERGIC RHINITIS

Allergic rhinitis involves an early phase, largely mediated through ma st cells, and a late phase which involves cellular infiltration and me diator release. In the early phase, mast cells release mediators as a result of antigen crosslinking adjacent immunoglobulin E molecules bou nd to mast cell surfaces. This results in an accumulation of histamine which gives rise to the characteristic symptoms of rhinitis - sneezin g, itching, rhinorrhoea and congestion. The late phase of the allergic response (hours after challenge) involves infiltration of the nasal e pithelium by eosinophils, basophils, monocytes and T-lymphocytes, whic h release leukotrienes, kinins, histamine and a host of other mediator s. The most important part of the late-phase response is probably medi ated via the production of cytokines (IL-4, IL-5, IL-6, IL-8, GM-CSF a nd RANTES) by mast cells, TH2 lymphocytes or epithelial cells. The inf iltration of tissues by cells normally present only in the blood is br ought about by the production of adhesion molecules, such as VCAM-1 an d E-selectin, which cause circulating eosinophils, basophils and T-lym phocytes to adhere to endothelial cells before moving through the endo thelium into the tissue (diapedesis). Neuronal reflexes also play a ro le in the allergic response, both by mediating local responses to medi ators 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, possib ly due to changes in osmolality of the nasal surface fluid. Similar fa ctors may play a role in the aetiology of non-allergic rhinitis.