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首页> 外文期刊>Clinical and experimental allergy : >Unique populations of lung mast cells are required for antigen-mediated bronchoconstriction.
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Unique populations of lung mast cells are required for antigen-mediated bronchoconstriction.

机译：抗原介导的支气管收缩需要独特的肺肥大细胞种群。

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BACKGROUND: Studies in both human and mouse indicate that mediators released by mast cells can lead to bronchoconstriction, and thus these are important effector cells in lifethreatening anaphylaxis. Much of our understanding of the various functions of mast cells emanates from the study of mice lacking these cells, particularly mice carrying mutations in the tyrosine kinase gene Kit. Definitive evidence for the role of mast cells in the altered immune response requires the demonstration that this response can be normalized by reconstitution of the mice with cultured bone marrow-derived mast cells (BMMCs). While many mast cell niches can be restored with BMMCs, this has not been demonstrated for mast cells present in the airways of the lung, cells poised to mediate bronchoconstriction during allergic responses. OBJECTIVE: To determine if mast cell-deficient Kit(Wsh/Wsh) reconstituted lines are an appropriate model for the study of the role of these cells in bronchoconstriction associated with allergic responses. METHODS: Kit(Wsh/Wsh) mice were reconstituted with either whole bone marrow (WBM) or BMMCs and responses to IgE-mediated mast cell activation were determined; including systemic hypothermia, mediator release, and bronchoconstriction in anaesthetized, mechanically ventilated animals. RESULTS: Engraftment of Kit(Wsh/Wsh) mice with WBM and BMMCs results in reconstitution of the central airways with mast cells. While the treatment of the two groups of animals resulted in systemic changes when challenged with IgE/Ag in a model of passive anaphylaxis, bronchoconstriction was observed only in kit(Wsh/Wsh) animals, which had received a bone marrow transplant. CONCLUSIONS: While BMMCs can populate the lung, they cannot restore IgE/Ag-mediated bronchoconstriction to mast cell-deficient animals. This suggests that the mast cell population, which mediates this function, may be unique, and to fill this niche in the lung cells must undergo a specific developmental programme, one that is no longer available to cultured mast cells.
机译：背景：在人类和小鼠中的研究表明，肥大细胞释放的介体可导致支气管收缩，因此它们是威胁生命的过敏反应中的重要效应细胞。我们对肥大细胞的各种功能的大部分理解源于对缺乏这些细胞的小鼠的研究，尤其是在酪氨酸激酶基因Kit中携带突变的小鼠。有关肥大细胞在改变的免疫反应中的作用的明确证据需要证明，可以通过用培养的骨髓源肥大细胞（BMMC）重建小鼠来使该反应正常化。尽管许多肥大细胞壁with可以用BMMC修复，但肺气道中存在的肥大细胞尚未得到证实，这些细胞准备在变态反应期间介导支气管收缩。目的：确定肥大细胞缺乏试剂盒（Wsh / Wsh）重组株是否是研究这些细胞在与变态反应相关的支气管收缩中作用的合适模型。方法：用全骨髓（WBM）或BMMC重组Kit（Wsh / Wsh）小鼠，并测定其对IgE介导的肥大细胞活化的反应。包括全身麻醉的，机械通气的动物的体温过低，介质释放和支气管收缩。结果：用WBM和BMMCs植入Kit（Wsh / Wsh）小鼠会导致肥大细胞重建中央气道。在被动过敏反应模型中，两组动物的治疗在受到IgE / Ag攻击时导致全身性变化，但仅在接受骨髓移植的成套件（Wsh / Wsh）动物中观察到支气管收缩。结论：尽管BMMCs可以在肺中分布，但它们无法恢复肥大细胞缺陷动物的IgE / Ag介导的支气管收缩。这表明介导此功能的肥大细胞群可能是独特的，并且为了填补肺细胞中的这一小生境，必须经历一种特定的发育程序，而培养的肥大细胞不再可用这种程序。

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