Cameron L A, Durham S R, Jacobson M R, Masuyama K, Juliusson S, Gould H J, Lowhagen O, Minshall E M, Hamid Q A
Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
J Allergy Clin Immunol. 1998 Mar;101(3):330-6. doi: 10.1016/s0091-6749(98)70244-1.
Nasal allergen provocation has demonstrated that allergen-induced rhinitis is associated with an increase in local IL-4 mRNA and IgE heavy chain (Cepsilon) and IgE heavy chain promoter (Iepsilon) RNA and that pretreatment with topical glucocorticosteroids inhibits the increase in these transcripts.
This study was undertaken to determine whether observations made after acute allergen provocation can be extended to the case of chronic exposure experienced during the pollen season.
Biopsy specimens were obtained from the inferior turbinate of 33 pollen-sensitive subjects with allergic rhinitis before and during pollen season. Patients were randomized in a double-blind fashion and treated with either topical steroids (200 microg fluticasone propionate twice daily; n = 16) or matched placebo nasal spray (n = 17) before the pollen season. Alkaline phosphatase anti-alkaline phosphatase immunocytochemistry was used to identify B cells (CD20+), and in situ hybridization was used to detect IL-4, Cepsilon, and Iepsilon RNA+ cells.
Baseline examination revealed IL-4 and Cepsilon RNA but virtually no Iepsilon RNA+ cells in the nasal mucosa. Analysis revealed a significant difference in the expression of Cepsilon and Iepsilon RNA+ cells (p < 0.001). Biopsy specimens taken after antigen exposure exhibited highly significant increases in placebo-treated (p < 0.001) but not steroid-treated patients. In both groups, the number of CD20+ cells was unchanged when preexposure and postexposure biopsy specimens were compared.
These results show strong support for the hypothesis that IgE class switching occurs locally within the nasal mucosa of subjects with seasonal allergic rhinitis and that this response can be inhibited through strategies directed against local IgE production.
鼻过敏原激发试验已表明，过敏原诱发的鼻炎与局部白细胞介素-4 mRNA、免疫球蛋白E重链（Cε）和免疫球蛋白E重链启动子（Iε）RNA的增加有关，且局部糖皮质激素预处理可抑制这些转录物的增加。
本研究旨在确定急性过敏原激发后观察到的结果是否可推广至花粉季节期间慢性暴露的情况。
在花粉季节之前和期间，从33名患有过敏性鼻炎的花粉敏感受试者的下鼻甲获取活检标本。患者以双盲方式随机分组，并在花粉季节前接受局部类固醇治疗（每日两次，每次200微克丙酸氟替卡松；n = 16）或匹配的安慰剂鼻喷雾剂治疗（n = 17）。使用碱性磷酸酶抗碱性磷酸酶免疫细胞化学鉴定B细胞（CD20+），并使用原位杂交检测白细胞介素-4、Cε和Iε RNA+细胞。
基线检查显示鼻黏膜中有白细胞介素-4和Cε RNA，但几乎没有Iε RNA+细胞。分析显示Cε和Iε RNA+细胞的表达存在显著差异（p < 0.001）。抗原暴露后采集的活检标本显示，安慰剂治疗组（p < 0.001）有高度显著增加，而类固醇治疗组则无。在两组中，比较暴露前和暴露后的活检标本时，CD20+细胞数量均未改变。
这些结果有力支持了以下假设：季节性过敏性鼻炎患者的鼻黏膜内局部发生免疫球蛋白E类别转换，且这种反应可通过针对局部免疫球蛋白E产生的策略加以抑制。
