Abstract
Histamine induces nasal allergy symptoms via histamine H1 receptor subtypes (H1Rs). H1Rs are up- and down-regulated depending on conditions, and the mechanisms are thought to be important in regulating histamine signaling. Previously, we developed a nasal hypersensitivity animal model involving guinea pigs sensitized to toluene 2,4-diisocyanate (TDI), and observed neurogenic inflammation in the nasal mucosa on exposure to TDI [1‐3]. In this study, we examined both the expression levels of H1R mRNAs and molecules in the nasal mucosa of TDI sensitized rats. H1R mRNA levels were determined by the quantitative real-time reverse-transcriptase polymerase chain reaction (RT-PCR) method. We also investigated the effect of d-chlorpheniramine (CHP) and dexamethasone (DEX) on TDI-induced H1R mRNA expression and nasal symptoms. Application of TDI led to an increase in H1R mRNA levels and pretreatment with CHP and DEX reversed the increase. Radioligand receptor binding assays revealed that H1R molecules were significantly up-regulated by TDI provocation.
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Schedule a callMore From: Inflammation research : official journal of the European Histamine Research Society ... [et al.]
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