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首页> 外文期刊>American Journal of Physiology >Th17 cells contribute to pulmonary fibrosis and inflammation during chronic kidney disease progression after acute ischemia
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Th17 cells contribute to pulmonary fibrosis and inflammation during chronic kidney disease progression after acute ischemia

机译：Th17细胞在急性缺血后慢性肾脏疾病进展期间有助于肺纤维化和炎症

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摘要

Acute kidney injury (AKI) is associated with high mortality rates and predisposes development of chronic kidney disease (CKD). Distant organ damage, particularly in the lung, may contribute to mortality in AKI patients. Animal models of AKI demonstrate an increase in pulmonary infiltration of lymphocytes and reveal an acute compromise of lung function, but the chronic effects of AKI on pulmonary inflammation are unknown. We hypothesized that in response to renal ischemia/reperfusion (I/R), there is a persistent systemic increase in Th17 cells with potential effects on pulmonary structure and function. Renal I/R injury was performed on rats, and CKD progression was hastened by unilateral nephrectomy and exposure to 4.0% sodium diet between 35 and 63 days post-I/R. Thl7 cells in peripheral blood showed a progressive increase up to 63 days after recovery from I/R injury. Infiltration of leukocytes including Th17 cells was also elevated in bronchiolar lavage (BAL) fluid 7 days after I/R and remained elevated for up to 63 days. Lung histology demonstrated an increase in alveolar cellularity and a significant increase in picrosirius red staining. Suppression of lymphocytes with mycophenolate mofetil (MMF) or an IL-17 antagonist significantly reduced Th17 cell infiltration and fibrosis in lung. In addition, tracheal smooth muscle contraction to acetylcholine was significantly enhanced 63-days after I/R relative to sham-operated controls. These data suggest that AKI is associated with a persistent increase in circulating and lung Th17 cells which may promote pulmonary fibrosis and the potential alteration in airway contractility.
机译：急性肾损伤（AKI）与慢性肾病（CKD）的高死亡率和易患发展有关。遥远的器官损伤，特别是在肺部，可能导致AKI患者的死亡率。 AKI的动物模型表明淋巴细胞肺浸润的增加，揭示了肺功能的急性折衷，但AKI对肺炎症的慢性效应未知。我们假设响应肾缺血/再灌注（I / R），Th17细胞存在持续全身增加，具有对肺结核结构和功能的潜在影响。对大鼠进行肾I / R损伤，通过单侧肾切除术，并在I / R后的35至63天内暴露于4.0％钠饮食中的CKD进展。周围血液中的TH17细胞显示在I / R损伤中恢复后逐渐增加63天。在I / R后7天，在支气管灌洗（BAL）液体中也升高了白细胞的浸润，并且在I / R后7天升高，持续高达63天。肺组织学展示了肺泡细胞性的增加和Picrosirius红染色的显着增加。用霉酚酸酯（MMF）或IL-17拮抗剂的淋巴细胞抑制显着降低了肺部的细胞浸润和纤维化。此外，在I / R相对于假手术控制后63天的气管平滑肌肉收缩显着提高了63天。这些数据表明，AKI与循环和肺部Th17细胞的持续增加有关，这可能促进肺纤维化和气道收缩性的潜在改变。

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