Characteristics and control of the upper airway remodeling

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The mechanisms by which nasal mucosa remodeling occurs in allergic rhinitis have remained unclear. The aim of this study was to establish a guinea pig model of allergic rhinitis with remodeling and to examine the effects of dexamethasone and pranlukast on nasal mucosa remodeling. Three groups of ovalbumin-sensitized Hartley guinea pigs received daily intranasal challenges with ovalbumin for 1, 8, 12 weeks, respectivelylb examine the effect of dexamethasone and pranlukast, the animals were divided into 4 groups : negative control group ; ovalbumin-sensitized group ; ovalbumin+dexamethasone gmup ; and ovalbumin+pranlukast group. During 12 weeks of intranasal exposure to ovalbumin, the latter two groups received daily intraperitoneal injections of dexamethasone and pranlukast, respectively. Prolonged ovalbumin challenge caused significant pathological changes in the nasal mucosa and conchae, including eosinophil infiltration, significant goblet cell hyperplasia, epithelial damage and deposition of extracellular matrix. In contrast to the negative control group, the ovalbumin-sensitized group exhibited significant goblet cell hyperplasia, epithelial damage and deposition of extracellular matrix. These changes were significantly inhibited by dexamethasone and pranlukast, respectively. We have established a model of upper airway remodeling in guinea pigs. The tissue remodeling was inhibited by early intervention with the and allergic-inflammatory agents dexamethasone and pranlukast