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Alveolar macrophage activation and an emphysema-like phenotype in adiponectin-deficient mice

机译:脂联素缺乏症小鼠的肺泡巨噬细胞活化和肺气肿样表型

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In this study, we set out to further investigate the functional role of adiponectin in the lung using mice that are adiponectin deficient by target gene disruption. Our findings show that adiponectin is present at high concentrations in bronchoalveo-lar lavage (BAL) fluid of wild-type mice and that complete or partial deficiency leads to structure changes in the lung characteristic of an emphysema-like phenotype. Proinflammatory cytokines and matrix metalloproteinases (MMPs) are increased in the lung of adiponectin-/- mice, and in vitro studies demonstrate that adiponectin acts to suppress alveolar macrophage activation and the release of MMPs. Together, our findings indicate that adiponectin plays an important role in lung immune cell homeostasis and suggest that adiponectin-deficient states may contribute to the pathogenesis of inflammatory lung conditions.
机译:在这项研究中,我们着手使用脂联素缺乏靶基因破坏的小鼠进一步研究脂联素在肺中的功能作用。我们的发现表明,脂联素以高浓度存在于野生型小鼠支气管肺泡灌洗(BAL)液中,完全或部分缺乏会导致肺气肿样表型的肺结构改变。脂联素-/-小鼠的肺中促炎性细胞因子和基质金属蛋白酶(MMPs)增加,并且体外研究表明脂联素可抑制肺泡巨噬细胞的活化和MMPs的释放。总之,我们的发现表明脂联素在肺免疫细胞稳态中起着重要作用,并表明脂联素缺乏状态可能与炎症性肺病的发病机理有关。

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