BACKGROUND: Histamine plays an important role in producing nasal symptoms via histamine H1 receptor (H1R) in allergic rhinitis. It is reported that the minimum histamine concentration that induces sneezing is lower in allergic patients than in normal control subjects. Previous studies by binding assay on H1R gave divided results on whether the number of H1Rs is increased in allergic rhinitis or not. OBJECTIVE: The objective of this study was to examine if H1R mRNA expression is increased in patients with allergic rhinitis compared with normal healthy volunteers. METHODS: We extracted RNA from scrapings of inferior turbinate mucosa of 10 patients suffering from allergic rhinitis and 10 control subjects. As the H1R gene lacks introns, we treated RNA pellets by DNase to distinguish RNA from contaminating genomic DNA. Since amplification of H1R and beta-actin mRNA remained in an exponential phase at 35 cycles, H1R and beta-actin mRNAs were amplified for 35 cycles by reverse transcription-polymerase chain reaction (RT-PCR). The PCR products were hybridized with internal probes and band intensities were quantitated by a densitometer. RESULTS: The mean +/- SD of H1R/beta-actin ratio was 0.88 +/- 0.62 for the patients with allergic rhinitis and 0.29 +/- 0.17 for the normal subjects; the difference was statistically significant (P < 0.01). CONCLUSIONS: These data suggest that expression of H1R mRNA is increased in the nasal mucosa of the patients with allergic rhinitis.
BACKGROUND:Histamine plays an important role in producing nasal symptoms via histamine H1 receptor (H1R) in allergic rhinitis. It is reported that the minimum histamine concentration that induces sneezing is lower in allergicpatients than in normal control subjects. Previous studies by binding assay on H1R gave divided results on whether the number of H1Rs is increased in allergic rhinitis or not. OBJECTIVE: The objective of this study was to examine if H1R mRNA expression is increased in patients with allergic rhinitis compared with normal healthy volunteers. METHODS: We extracted RNA from scrapings of inferior turbinate mucosa of 10 patients suffering from allergic rhinitis and 10 control subjects. As the H1R gene lacks introns, we treated RNA pellets by DNase to distinguish RNA from contaminating genomic DNA. Since amplification of H1R and beta-actin mRNA remained in an exponential phase at 35 cycles, H1R and beta-actin mRNAs were amplified for 35 cycles by reverse transcription-polymerase chain reaction (RT-PCR). The PCR products were hybridized with internal probes and band intensities were quantitated by a densitometer. RESULTS: The mean +/- SD of H1R/beta-actin ratio was 0.88 +/- 0.62 for the patients with allergic rhinitis and 0.29 +/- 0.17 for the normal subjects; the difference was statistically significant (P < 0.01). CONCLUSIONS: These data suggest that expression of H1R mRNA is increased in the nasal mucosa of the patients with allergic rhinitis.