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首页> 外文期刊>Clinical and experimental allergy : >Glutamine preferentially inhibits T-helper type 2 cell-mediated airway inflammation and late airway hyperresponsiveness through the inhibition of cytosolic phospholipase A(2) activity in a murine asthma model.
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Glutamine preferentially inhibits T-helper type 2 cell-mediated airway inflammation and late airway hyperresponsiveness through the inhibition of cytosolic phospholipase A(2) activity in a murine asthma model.

机译：谷氨酰胺通过抑制鼠哮喘模型中的胞质磷脂酶A（2）活性，优先抑制T型辅助2型细胞介导的气道炎症和晚期气道高反应性。

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摘要

BACKGROUND: The non-essential amino acid, l-glutamine (Gln), is abundant in the human body. Gln exhibits beneficial effects on endotoxic shock through the inhibition of cytosolic phospholipase A(2) (cPLA(2)) activity. cPLA(2) has been reported to be implicated in the pathogenesis of asthma, but the effects of Gln on asthma have not yet been defined. OBJECTIVE: To investigate the effects of Gln on allergic bronchial inflammation and airway hyperresponsiveness (AHR), and to determine the possible action mechanisms of Gln in a murine model of asthma. METHODS: cPLA(2) phosphorylation was assessed by immunoprecipitation and Western blotting. Smears of bronchoalveolar lavage cells were stained with Diff-Quik solution for differential cell counting. Airway levels of the proteins [T-helper type-1 (Th1) and Th2 cytokines, and mucin] were measured by ELISA. mRNA expression of cytokines was assessed by real-time RT-PCR. AHR was assessed as a change in airway resistance (RL). Histological studies were performed to assess the levels of mucin and pulmonary inflammation. RESULTS: Systemic Gln administration inhibited cPLA(2) phosphorylation and its enzymatic activity in the lungs. Additionally, Gln effectively suppressed the key features of Th2-dependent asthmatic features, such as airway eosinophilia, mucus formation, and airway type 2 cytokine production, as well as late AHR. CONCLUSION: Gln was found to be effective in the suppression of Th2-dependent phenotypes and late AHR, and this effect of Gln appeared to be at least partially attributable to its ability to suppress cLPA(2) activity in the airway. Our results suggest that clinical use of Gln for patients with asthma may be beneficial.
机译：背景：非必需氨基酸l-谷氨酰胺（Gln）在人体中含量很高。 Gln通过抑制胞质磷脂酶A（2）（cPLA（2））的活性对内毒素休克表现出有益的作用。据报道，cPLA（2）与哮喘的发病机制有关，但尚未确定Gln对哮喘的作用。目的：研究Gln对过敏性支气管炎症和气道高反应性（AHR）的影响，并确定Gln在哮喘小鼠模型中的可能作用机制。方法：通过免疫沉淀和蛋白质印迹法评估cPLA（2）的磷酸化。支气管肺泡灌洗细胞涂片用Diff-Quik溶液染色以进行细胞计数。通过ELISA测量蛋白质的气道水平[T-辅助1型（Th1）和Th2细胞因子以及粘蛋白]。通过实时RT-PCR评估细胞因子的mRNA表达。 AHR被评估为气道阻力（RL）的变化。进行组织学研究以评估粘蛋白和肺部炎症的水平。结果：全身Gln给药抑制了cPLA（2）磷酸化及其在肺中的酶活性。此外，Gln有效抑制Th2依赖性哮喘特征的关键特征，例如气道嗜酸性粒细胞增多，粘液形成，气道2型细胞因子生成以及晚期AHR。结论：发现Gln可有效抑制Th2依赖型和晚期AHR，Gln的这种作用似乎至少部分归因于其抑制气道cLPA（2）活性的能力。我们的结果表明，Gln在哮喘患者中的临床应用可能是有益的。

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