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Airway eosinophilic inflammation is attenuated in conserved noncoding sequence-1-deficient mice.

机译:在保守的非编码序列-1缺陷小鼠中,气道嗜酸性炎症减弱。

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BACKGROUND: Conserved noncoding sequence-1 (CNS-1) is an important regulatory element for T helper 2 cytokine expression. IL-4, IL-5 and IL-13 expression as well as serum IgE level were attenuated in CNS-1-/- mice. METHOD: CNS-1-/- and CNS-1+/+ mice were sensitized with ovalbumin (OVA) followed by antigen challenge. The number of eosinophils and T helper 2 cytokine concentration in the bronchoalveolar lavage fluid, OVA-specific IgE antibody (Ab) in the serum and bronchial responsiveness to methacholine were examined. RESULTS: Bronchoalveolar lavage fluid eosinophilia was significantly attenuated in CNS-1-/- mice compared to CNS-1+/+ mice, which were sensitized with OVA/aluminum once. OVA-specific IgE Ab was also attenuated. When mice were sensitized with OVA/aluminum twice, induction of eosinophilia and OVA-specific IgE Ab was not significantly different between CNS-1-/- and CNS-1+/+ mice. CONCLUSION: CNS-1 locus regulates eosinophilic inflammation in vivo.
机译:背景:保守的非编码序列1(CNS-1)是T辅助2细胞因子表达的重要调控元件。在CNS-1-/-小鼠中,IL-4,IL-5和IL-13的表达以及血清IgE水平降低。方法:用卵清蛋白(OVA)致敏CNS-1-/-和CNS-1 + / +小鼠,然后进行抗原攻击。检查支气管肺泡灌洗液中嗜酸性粒细胞和T辅助2细胞因子的浓度,血清中OVA特异性IgE抗体(Ab)以及支气管对乙酰甲胆碱的反应性。结果:与用OVA /铝敏化的CNS-1 + / +小鼠相比,CNS-1-/-小鼠的支气管肺泡灌洗液嗜酸性粒细胞减少明显。 OVA特异性IgE抗体也被减弱。当用OVA /铝敏化小鼠两次时,CNS-1-/-和CNS-1 + / +小鼠的嗜酸性粒细胞增多和OVA特异性IgE Ab的诱导没有显着差异。结论:CNS-1基因座在体内调节嗜酸性炎症。

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