PDF(Pubmed)
Abstract：
UNASSIGNED: Group 2 innate lymphoid cells (ILC2s) have been found to take part in type 2 inflammation by secreting TH2 cytokines. Apolipoprotein A-I (Apo-AI), a major structural and functional protein of high-density lipoproteins, has anti-inflammatory effects on neutrophils, monocytes, macrophages, and eosinophils. However, its effects on ILC2s are not well characterized.
UNASSIGNED: We aimed to investigate the effect of Apo-AI on the proliferation and function of ILC2s as well as its possible mechanism.
UNASSIGNED: The protein expression of Apo-AI and the percentage of ILC2s in peripheral blood between 20 allergic rhinitis patients and 20 controls were detected by ELISA and flow cytometry. The effect of Apo-AI and miR-155 on ILC2 proliferation and function was detected by tritiated thymidine incorporation and ELISA. Anima models were adopted to verify the effect of Apo-AI in vivo.
UNASSIGNED: Elevated expression of Apo-AI was observed in allergic rhinitis patients. Apo-AI promotes ABCA1 expression by ILC2s, which can be inhibited by anti-Apo-AI. Apo-AI decreased ILC2 proliferation and the microRNA levels of GATA3 and RORα from ILC2s. The miR-155 overexpression promoted the upregulation of GATA3 and type II cytokines from ILC2s, while the addition of Apo-AI or miR-155 inhibitor significantly inhibited expression of GATA3 and type II cytokines by ILC2s. Apo-AI-/- mice showed as enhanced allergen-induced airway inflammation. The miR-155 inhibitor can reverse the enhanced allergen-induced airway inflammation in Apo-AI-/- mice, while miR-155 mimics can reverse the decreased allergen-induced airway inflammation in Apo-AI-treated mice.
UNASSIGNED: Apo-AI suppressed the proliferation and function of ILC2s through miR-155 in allergic rhinitis. Our data provide new insights into the mechanism of allergen-induced airway inflammation.
UNASSIGNED: We aimed to investigate the effect of Apo-AI on the proliferation and function of ILC2s as well as its possible mechanism.
UNASSIGNED: The protein expression of Apo-AI and the percentage of ILC2s in peripheral blood between 20 allergic rhinitis patients and 20 controls were detected by ELISA and flow cytometry. The effect of Apo-AI and miR-155 on ILC2 proliferation and function was detected by tritiated thymidine incorporation and ELISA. Anima models were adopted to verify the effect of Apo-AI in vivo.
UNASSIGNED: Elevated expression of Apo-AI was observed in allergic rhinitis patients. Apo-AI promotes ABCA1 expression by ILC2s, which can be inhibited by anti-Apo-AI. Apo-AI decreased ILC2 proliferation and the microRNA levels of GATA3 and RORα from ILC2s. The miR-155 overexpression promoted the upregulation of GATA3 and type II cytokines from ILC2s, while the addition of Apo-AI or miR-155 inhibitor significantly inhibited expression of GATA3 and type II cytokines by ILC2s. Apo-AI-/- mice showed as enhanced allergen-induced airway inflammation. The miR-155 inhibitor can reverse the enhanced allergen-induced airway inflammation in Apo-AI-/- mice, while miR-155 mimics can reverse the decreased allergen-induced airway inflammation in Apo-AI-treated mice.
UNASSIGNED: Apo-AI suppressed the proliferation and function of ILC2s through miR-155 in allergic rhinitis. Our data provide new insights into the mechanism of allergen-induced airway inflammation.
摘要：
■已发现第2组先天淋巴样细胞（ILC2s）通过分泌TH2细胞因子参与2型炎症。载脂蛋白A-I(Apo-AI),高密度脂蛋白的主要结构和功能蛋白，对中性粒细胞有抗炎作用，单核细胞,巨噬细胞，和嗜酸性粒细胞.然而,它对ILC2的影响没有很好的表征。
■我们旨在研究Apo-AI对ILC2s增殖和功能的影响及其可能的机制。
■采用ELISA和流式细胞术检测20例变应性鼻炎患者和20例对照者外周血中Apo-AI的蛋白表达和ILC2s的百分比。通过氚化胸苷掺入和ELISA检测Apo-AI和miR-155对ILC2增殖和功能的影响。采用Anima模型验证Apo-AI的体内效果。
■在变应性鼻炎患者中观察到Apo-AI的表达升高。Apo-AI通过ILC2s促进ABCA1表达，可以被抗Apo-AI抑制。Apo-AI降低ILC2增殖以及来自ILC2s的GATA3和RORα的microRNA水平。miR-155过表达促进了来自ILC2s的GATA3和II型细胞因子的上调,而Apo-AI或miR-155抑制剂的添加显着抑制了ILC2s对GATA3和II型细胞因子的表达。Apo-AI-/-小鼠表现为增强的变应原诱导的气道炎症。miR-155抑制剂可逆转Apo-AI-/-小鼠变应原诱导的气道炎症,而miR-155模拟物可以逆转Apo-AI治疗小鼠中变应原诱导的气道炎症的减少。
■Apo-AI在变应性鼻炎中通过miR-155抑制ILC2s的增殖和功能。我们的数据为过敏原诱导的气道炎症的机制提供了新的见解。
■我们旨在研究Apo-AI对ILC2s增殖和功能的影响及其可能的机制。
■采用ELISA和流式细胞术检测20例变应性鼻炎患者和20例对照者外周血中Apo-AI的蛋白表达和ILC2s的百分比。通过氚化胸苷掺入和ELISA检测Apo-AI和miR-155对ILC2增殖和功能的影响。采用Anima模型验证Apo-AI的体内效果。
■在变应性鼻炎患者中观察到Apo-AI的表达升高。Apo-AI通过ILC2s促进ABCA1表达，可以被抗Apo-AI抑制。Apo-AI降低ILC2增殖以及来自ILC2s的GATA3和RORα的microRNA水平。miR-155过表达促进了来自ILC2s的GATA3和II型细胞因子的上调,而Apo-AI或miR-155抑制剂的添加显着抑制了ILC2s对GATA3和II型细胞因子的表达。Apo-AI-/-小鼠表现为增强的变应原诱导的气道炎症。miR-155抑制剂可逆转Apo-AI-/-小鼠变应原诱导的气道炎症,而miR-155模拟物可以逆转Apo-AI治疗小鼠中变应原诱导的气道炎症的减少。
■Apo-AI在变应性鼻炎中通过miR-155抑制ILC2s的增殖和功能。我们的数据为过敏原诱导的气道炎症的机制提供了新的见解。
