Iriyoshi N, Takeuchi K, Yuta A, Ukai K, Sakakura Y
Department of Otorhinolaryngology, Mie University School of Medicine, Japan.
Clin Exp Allergy. 1996 Apr;26(4):379-85.
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.
The objective of this study was to examine if H1R mRNA expression is increased in patients with allergic rhinitis compared with normal healthy volunteers.
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.
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).
These data suggest that expression of H1R mRNA is increased in the nasal mucosa of the patients with allergic rhinitis.
组胺通过组胺H1受体（H1R）在变应性鼻炎中产生鼻部症状方面发挥重要作用。据报道，诱导打喷嚏的最低组胺浓度在变应性患者中低于正常对照受试者。先前通过H1R结合试验进行的研究对于变应性鼻炎中H1R数量是否增加给出了不一致的结果。
本研究的目的是检查与正常健康志愿者相比，变应性鼻炎患者中H1R mRNA表达是否增加。
我们从10例变应性鼻炎患者和10例对照受试者的下鼻甲黏膜刮片中提取RNA。由于H1R基因缺乏内含子，我们用DNase处理RNA沉淀以区分RNA与污染的基因组DNA。由于H1R和β-肌动蛋白mRNA在35个循环时仍处于指数期，通过逆转录聚合酶链反应（RT-PCR）对H1R和β-肌动蛋白mRNA进行35个循环的扩增。PCR产物与内部探针杂交，并用密度计对条带强度进行定量。
变应性鼻炎患者的H1R/β-肌动蛋白比值的平均值±标准差为0.88±0.62，正常受试者为0.29±0.17；差异具有统计学意义（P<0.01）。
这些数据表明变应性鼻炎患者鼻黏膜中H1R mRNA的表达增加。
