首页> 美国卫生研究院文献>Immunology >Topical glucocorticosteroid (fluticasone propionate) inhibits cells expressing cytokine mRNA for interleukin-4 in the nasal mucosa in allergen-induced rhinitis.
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Topical glucocorticosteroid (fluticasone propionate) inhibits cells expressing cytokine mRNA for interleukin-4 in the nasal mucosa in allergen-induced rhinitis.

机译:局部用糖皮质激素(丙酸氟替卡松)抑制变应原诱导的鼻炎患者鼻黏膜中表达白细胞介素-4的细胞因子mRNA的细胞。

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摘要

Allergen-induced late nasal responses are associated with recruitment and activation of T lymphocytes and eosinophils and preferential mRNA expression for T-helper type 2 (Th2) cytokines. We tested the hypothesis that topical corticosteroids may inhibit late responses by inhibiting cells expressing mRNA for Th2 cytokines. A randomized double-blind placebo-controlled trial of topical corticosteroid (fluticasone propionate) was performed in 48 adult grass pollen-sensitive patients. Nasal biopsies were taken at baseline and repeated 24 hr after local nasal allergen provocation following 6 weeks treatment with either fluticasone propionate 200 micrograms or placebo nasal spray twice daily. Baseline mRNA expression for interleukin-4 (IL-4) (P = 0.01) and IL-5 (P = 0.002) was higher in the patients than in normal controls. Topical corticosteroid treatment significantly inhibited immediate nasal symptoms, with almost complete inhibition of the late response following allergen challenge. This was associated with a marked decrease in the allergen-induced increases in cells expressing mRNA for IL-4 (P = 0.002) but not for IL-5. Inhibition of the late response was also accompanied by decreases in CD25+ cells, presumed T lymphocytes and eosinophils. A significant correlation was observed between the decreases in IL-4 mRNA+ cells and in eosinophils after treatment (r = 0.46, P < 0.05). These results suggest that prolonged treatment with topical corticosteroid inhibits allergen-induced early and late nasal responses and the associated tissue eosinophilia, and that, at least in part, this may result from inhibition of cells expressing mRNA for IL-4.
机译:变应原诱导的晚期鼻腔反应与T淋巴细胞和嗜酸性粒细胞的募集和激活以及T型辅助2型(Th2)细胞因子的优先mRNA表达有关。我们测试了局部皮质类固醇可能通过抑制表达Th2细胞因子mRNA的细胞来抑制晚期反应的假说。在48名成年对花粉敏感的成年患者中进行了局部皮质类固醇(丙酸氟替卡松)的随机双盲安慰剂对照试验。在基线时进行鼻活检,并在每天两次用丙酸氟替卡松200毫克或安慰剂鼻喷雾剂治疗6周后,在局部鼻过敏原激发后24小时重复进行。患者的白细胞介素4(IL-4)和IL-5(P = 0.002)的基线mRNA表达高于正常对照组。局部皮质类固醇激素治疗显着抑制了鼻部症状,几乎完全抑制了过敏原激发后的晚期反应。这与IL-4表达mRNA的细胞中变应原诱导的表达的显着减少有关(P = 0.002),但IL-5表达却没有。晚期应答的抑制还伴随着CD25 +细胞,推测的T淋巴细胞和嗜酸性粒细胞减少。在治疗后,IL-4 mRNA +细胞的减少与嗜酸性粒细胞的减少之间存在显着相关性(r = 0.46,P <0.05)。这些结果表明,长期用局部皮质类固醇激素治疗可抑制变应原诱导的早期和晚期鼻腔反应以及相关的组织嗜酸性粒细胞增多,并且至少部分地,这可能是由于抑制表达IL-4 mRNA的细胞所致。

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