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首页> 外文期刊>Infection and immunity >Pseudomonas aeruginosa Alginate Promotes Burkholderia cenocepacia Persistence in Cystic Fibrosis Transmembrane Conductance Regulator Knockout Mice
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Pseudomonas aeruginosa Alginate Promotes Burkholderia cenocepacia Persistence in Cystic Fibrosis Transmembrane Conductance Regulator Knockout Mice

机译：铜绿假单胞菌藻酸盐促进囊性伯克霍尔德氏菌持续存在于囊性纤维化中跨膜电导调节剂敲除小鼠

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Pseudomonas aeruginosa, a major respiratory pathogen in cystic fibrosis (CF) patients, facilitates infection by other opportunistic pathogens. Burkholderia cenocepacia, which normally infects adolescent patients, encounters alginate elaborated by mucoid P. aeruginosa. To determine whether P. aeruginosa alginate facilitates B. cenocepacia infection in mice, cystic fibrosis transmembrane conductance regulator knockout mice were infected with B. cenocepacia strain BC7 suspended in either phosphate-buffered saline (BC7/PBS) or P. aeruginosa alginate (BC7/alginate), and the pulmonary bacterial load and inflammation were monitored. Mice infected with BC7/PBS cleared all of the bacteria within 3 days, and inflammation was resolved by day 5. In contrast, mice infected with BC7/alginate showed persistence of bacteria and increased cytokine levels for up to 7 days. Histological examination of the lungs indicated that there was moderate to severe inflammation and pneumonic consolidation in isolated areas at 5 and 7 days postinfection in the BC7/alginate group. Further, alginate decreased phagocytosis of B. cenocepacia by professional phagocytes both in vivo and in vitro. P. aeruginosa alginate also reduced the proinflammatory responses of CF airway epithelial cells and alveolar macrophages to B. cenocepacia infection. The observed effects are specific to P. aeruginosa alginate, because enzymatically degraded alginate or other polyuronic acids did not facilitate bacterial persistence. These observations suggest that P. aeruginosa alginate may facilitate B. cenocepacia infection by interfering with host innate defense mechanisms.
机译：铜绿假单胞菌是囊性纤维化（CF）患者的主要呼吸道病原体，有助于其他机会性病原体的感染。通常感染青春期患者的 Burkholderia cenocepacia 会遇到由黏液状蛋白 P精心制作的藻酸盐。铜绿。确定是否 P。铜绿藻藻酸盐促进 B。小鼠感染新陈代谢后， B感染了囊性纤维化跨膜电导调节剂敲除小鼠。革兰氏菌BC7菌株悬浮在磷酸盐缓冲液（BC7 / PBS）或 P中。监测铜绿藻藻酸盐（BC7 /藻酸盐）的含量，并监测其肺部细菌负荷和炎症。感染BC7 / PBS的小鼠在3天内清除了所有细菌，并在第5天消退了炎症。相比之下，感染BC7 /藻酸盐的小鼠在7天内表现出细菌的持久性并增加了细胞因子水平。肺的组织学检查表明，在BC7 /藻酸盐组感染后第5天和第7天，在偏远地区存在中度至重度的炎症和肺炎巩固。此外，藻酸盐降低了 B的吞噬作用。通过专业吞噬细胞在体内 和体外进行大菌血症。铜绿假单胞菌藻酸盐还降低了CF气道上皮细胞和肺泡巨噬细胞对 B的促炎反应。洋葱感染观察到的效果特定于 P。铜绿藻藻酸盐，因为酶促降解的藻酸盐或其他聚糖醛酸不能促进细菌的持久性。这些发现表明 P。铜绿藻藻酸盐可能促进 B。通过干扰宿主的先天防御机制来感染新陈皮。

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