| Allergic rhinitis is characterized by nasal mucosal inflammation resulting from seasonal or perennial responses to allergens. Symptoms of allergic rhinitis are sneezing, rhinorrhea, nasal congestion, and nasal itching are often present, and studies have indicated that some patients with allergic rhinitis and no clinical evidence of asthma also exihibit airway hyperreactivity (AHR). These symptoms are considered to be caused by chemokine eotaxin and immunoglobulin E (IgE) -mediated activation of eosinophils from circulation and mucosal mast cells that are located on the epithelia of the nasal cavity. Most allergic rhinitis have eosinophils in their secretions and their associated mediators, which are probably associated with many of the allergic manifestations. The accumulation of eosinophils within the nasal mucosa is a characteristic feature of allergic rhinitis. Once degranulation of eosinophils within the mucosa releases granule constituents such as major basic protein, eosinophil cationic protein and eosinophil peroxidase, that can effect tissue damage and are thought to be important in the underlying AHR that is a hallmark of human rhinitis and asthma. Although mediators with chemoattractant activity towards eosinophils had been described, none showed selective effects on eosinophils until the discovery of the chemokine family. Eotaxin is a small protein that is produced in the nasal mucosa or lung of rhinitis or asthmatic patients and is a potent chemoattractant for eosinophils. Eotaxin, a CC chemokine, stimulates the migration of eosinophils from the small blood vessels in the nasal mucosa or lungs by acting on the CC chemokinereceptor CCR3 which is located on the leukocyte cell surface. The increasing prevalence of allergic rhinitis, its impact on individual quality of life and social costs, as well as its role as a risk factor for asthma, underline the need for improved treatment options for this disorder. In addition to well established pharmacological therapies with antihistamines, corticosteroids, decongestants and mast cell stabilizers, new therapeutic options become increasingly important, including leukotriene modifiers, anti-immunoglobulin E antibodies, phosphodiesterase inhibitors, intranasal heparin and cytokine receptor antagonist. Recently, some low molecular weight compounds have been developed that can block eotaxin receptor. Such compounds may be developed into orally available drugs aimed at preventing eosinophil recruitment and, hence, inhibiting the pathological process associated with the activation of these cells within the tissues. In the past studies, we fovnd that Cryptoporus polysaccharide (CP), a low molecular weight acid polysaccharide and multi-target anti-inflammatory effects isolated from Cryptoporus volvatus, showed inhibitory effects on Schultz-Dale constriction reaction of airway smooth muscle induced by antigen, leukotriene D4 (LTD4) production from guinea pigs lung stimulated by calcimycin in vitro and airway hyperresponsiveness by stabilizing mast cell membranes and reducing infiltration of eosinophils in airway tissue in vivo. Recent studies demostrated CP significantly inhibited airway constriction and EPO (eosinophil peroxidase) release from eosinophil in asthmatic model of guinea trig and inhibited eosinophil chemotaxis. It is now recognized that allergic rhinitis and asthma are two clinical manifestations of a single disorder of the airways, because of the close linkage between the upper and lower respiratory tracts. Inflammatory changes appear frequently in the lower airway of the patients with allergic rhinitis. More than half of the population with allergic rhinitis also has asthma. Allergic rhinitis is a risk factor for the development of asthma. In the present study, we evaluate whether CP can decrease the development of nasal symptoms, inhibit AHR to methylcholine and the infiltration of eosinophils in nasal mucosa in rat model of allergic rhinitis. In addition, we investigated a possible action mechanism of CP by detecting t...
|
PDF Full Text Request