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首页> 外文期刊>American Journal of Physiology >LPS-induced bronchial hyperreactivity: interference by mIL-10 differs according to site of delivery.
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LPS-induced bronchial hyperreactivity: interference by mIL-10 differs according to site of delivery.

机译：LPS诱导的支气管高反应性：mIL-10的干扰因递送部位而异。

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When administered to mice systemically or via the airways, LPS induces bronchoconstriction (BC) and/or bronchopulmonary hyperreactivity (BHR), associated with inflammation. Accordingly, a relationship between inflammation and allergic and nonallergic BHR can be hypothesized. We therefore studied the interference of the anti-inflammatory cytokine murine IL-10 (mIL-10) with LPS-induced lung inflammation, BC, and BHR. mIL-10 was administered directly into the airways by intranasal instillation or generated in vivo after muscle electrotransfer of mIL-10-encoding plasmid. Electrotransfer led to high mIL-10 circulating levels for a longer time than after the injection of recombinant mIL-10 (rmIL-10). rmIL-10 administered intranasally reduced lung inflammation and BHR after LPS administration into airways. It also reduced the ex vivo production of TNF-alpha by LPS-stimulated lung tissue explants. Two days after electrotransfer, mIL-10 blood levels were elevated, but lung inflammation, BC, and BHR persisted unaffected. Blood mIL-10 reaches the airways poorly, which probably accounts for the ineffectiveness of mIL-10-encoding plasmid electrotransfer. When LPS was aerosolized 15 days after electrotransfer, lung inflammation persisted but BHR was significantly reduced, an effect that may be related to the longer exposure of the relevant cells to mIL-10. The dissociation between inflammation and BHR indicates that both are not directly correlated. In conclusion, this study shows that mIL-10 is efficient against BHR when present in the airway compartment. Despite this, the muscle electrotransfer with mIL-10-encoding plasmid showed a protective effect against BHR after a delay of 2 wk that should be further investigated.
机译：当对小鼠全身或通过气道给药时，LPS会诱发与炎症相关的支气管收缩（BC）和/或支气管肺反应过度（BHR）。因此，可以推测炎症与过敏性和非过敏性BHR之间的关系。因此，我们研究了抗炎细胞因子鼠IL-10（mIL-10）对LPS诱导的肺部炎症，BC和BHR的干扰。通过鼻内滴注将mIL-10直接给药至气道，或在肌肉电转移mIL-10编码质粒后在体内产生mIL-10。与注射重组mIL-10（rmIL-10）后相比，电转移导致更长的时间产生较高的mIL-10循环水平。 LPIL进入呼吸道后，鼻内给予rmIL-10可减轻肺部炎症和BHR。它也减少了LPS刺激的肺组织外植体离体产生TNF-α。电转移后两天，mIL-10血液水平升高，但肺部炎症，BC和BHR持续存在，未受影响。血液mIL-10到达呼吸道的能力很差，这可能是mIL-10-编码质粒电转移无效的原因。当电转移后15天将LPS气雾化时，肺部炎症持续存在，但BHR显着降低，这可能与相关细胞长时间暴露于mIL-10有关。炎症和BHR之间的分离表明两者并不直接相关。总之，这项研究表明mIL-10在气道隔室内存在时对BHR有效。尽管如此，延迟2周后，用mIL-10-编码质粒进行的肌肉电转移仍显示出对BHR的保护作用，应进一步研究。

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