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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >Inhalation of alkylating mustard causes long-term T cell-dependent inflammation in airways and growth of connective tissue.
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Inhalation of alkylating mustard causes long-term T cell-dependent inflammation in airways and growth of connective tissue.

机译：吸入烷基化芥末会引起气道中长期依赖T细胞的炎症以及结缔组织的生长。

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Low-dose exposure of alkylating mustard gas causes long-term respiratory complications characterized by bronchitis and lung fibrosis. In this study, we utilized a mouse model for lung exposure of the nitrogen mustard melphalan, in order to define early and late events in the pathogenesis such as expression of pro-inflammatory cytokines, recruitment of inflammatory cells to airways and late-phase fibrosis. We investigated the roles of different T lymphocyte subsets on the inflammatory response by using knockout mice lacking either the genes expressing T cell receptor (TCR)alphabeta or TCRgammadelta, and compared the responsiveness with that of wild type mice and double knockout mice completely deficient in T cells. Exposure to melphalan induced an early burst of the pro-inflammatory cytokines interleukin (IL)-1beta, IL-6 and IL-23 in airways, followed by extensive infiltration of neutrophils in the lung tissue and airways within 24h. The acute phase was followed by a sustained lymphocytic response that persisted for at least 14 days with resulting lung fibrosis. Engagement of T lymphocytes, particularly the gammadelta T cell subset, was crucial both for the acute cytokine and neutrophil response and for the late-phase lung fibrosis as indicated by the lack of response in gammadelta T cell deficient mice. Our data demonstrate that T lymphocytes play a prominent role in the pathogenesis of long-term lung injuries caused by strong alkylating agents.
机译：低剂量暴露于烷基化芥菜气会导致长期呼吸道并发症，其特征在于支气管炎和肺纤维化。在这项研究中，我们利用小鼠氮芥芥子气暴露于肺的模型，以定义发病机制中的早期和晚期事件，例如促炎性细胞因子的表达，炎症细胞向气道的募集和晚期纤维化。我们使用缺乏表达T细胞受体（TCR）alphabeta或TCRgammadelta的基因的基因敲除小鼠研究了不同T淋巴细胞亚群在炎症反应中的作用，并将其与野生型小鼠和完全缺乏T细胞的双重基因敲除小鼠的反应性进行了比较。细胞。暴露于美法仑可导致气道中促炎性细胞因子白介素（IL）-1β，IL-6和IL-23的早期爆发，随后在24h内肺组织和气道中性粒细胞大量浸润。急性期之后是持续的淋巴细胞反应，持续至少14天，导致肺纤维化。 T淋巴细胞的参与，特别是γδT细胞亚群的参与，对于急性细胞因子和中性粒细胞反应以及晚期肺纤维化均至关重要，这是由于γδT细胞缺陷小鼠缺乏反应所致。我们的数据表明，T淋巴细胞在强烷基化剂引起的长期肺损伤的发病机理中起着重要作用。

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