Nasal hyperreactivity and inflammation in allergic rhinitis

Abstract

The history of allergic disease goes back to 1819, when Bostock described his own ‘periodical affection of the eyes and chest’, which he called ‘summer catarrh’. Since they thought it was produced by the effluvium of new hay, this condition was also called hay fever. Later, in 1873, Blackley established that pollen played an important role in the causation of hay fever. Nowadays, the definition of allergy is ‘An untoward physiologic event mediated by a variety of different immunologic reactions’. In this review, the term allergy will be restricted to the IgE-dependent reactions. The most important clinical manifestations of IgE-dependent reactions are allergic conjunctivitis, allergic rhinitis, allergic asthma and atopic dermatitis. However, this review will be restricted to allergic rhinitis. The histopathological features of allergic inflammation involve an increase in blood flow and vascular permeability, leading to plasma exudation and the formation of oedema. In addition, a cascade of events occurs which involves a variety of inflammatory cells. These inflammatory cells migrate under the influence of chemotactic agents to the site of injury and induce the process of repair. Several types of inflammatory cells have been implicated in the pathogenesis of allergic rhinitis. After specific or nonspecific stimuli, inflammatory mediators are generated from cells normally found in the nose, such as mast cells, antigen-presenting cells and epithelial cells (primary effector cells) and from cells recruited into the nose, such as basophils, eosinophils, lymphocytes, platelets and neutrophils (secondary effector cells). This review describes the identification of each of the inflammatory cells and their mediators which play a role in the perennial allergic processes in the nose of rhinitis patients.

Effect of Oral Immunotherapy on Nasal Blockage in Experimental Allergic Rhinitis

“…Thus, the inhibition of the biphasic nasal blockage by the immunotherapy may be due to the suppression on the development of nasal hyperresponsiveness. It has been indicated that nasal blockage is induced mainly by both dilatation of nasal blood vessels and increased vascular permeability (24). We have demonstrated that both the antigen-(25) and the LTD 4 -(15) induced nasal blockages in the sensitized guinea pig were largely inhibited by a vasoconstrictive α-adrenergic agonist, naphazoline.…”

Alterations of Vasoactive Intestinal Polypeptide Receptors in Allergic Rhinitis

“…The proposed hypothesis is increased permeability and increased sensitivity of sensory nerve endings and an imbalance of the autonomic nerve regulation caused by changes of the neuroreceptors in the nasal mucosa. 18 Megen et al 19 reported an increased sensitivity and a decreased number of muscarinic receptors in the nasal mucosa of allergic rhinitis. 19 With our results, we postulate that increased expression of VIP receptors could partially explain the hyperresponsiveness to nonspecific irritants in patients with allergic rhinitis.…”

“…18 Megen et al 19 reported an increased sensitivity and a decreased number of muscarinic receptors in the nasal mucosa of allergic rhinitis. 19 With our results, we postulate that increased expression of VIP receptors could partially explain the hyperresponsiveness to nonspecific irritants in patients with allergic rhinitis.…”

28-Day Repeated Oral Toxicity Study and Efficacy of a Siddha Polyherbal Formulation - Singinatha Choornam against Platelet Activating Factor-induced Rhinosinusitis in Wistar Albino Rat

“…PAF is an important inflammatory mediator of allergic rhinosinusitis which induce vascular leakage and lead to rhinorrhea formation and congestion [10] . For inducing rhinosinusitis in animal model, PAF is administered through nasal orifice which stimulates mast cell in nasal mucosa and increase the neutrophlis and eosinophils content [11] .…”