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首页> 外文期刊>Infection and immunity >The interleukin-1 receptor antagonist can either reduce or enhance the lethality of Klebsiella pneumoniae sepsis in newborn rats.
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The interleukin-1 receptor antagonist can either reduce or enhance the lethality of Klebsiella pneumoniae sepsis in newborn rats.

机译：白介素-1受体拮抗剂可以减少或增强新生大鼠肺炎克雷伯菌败血症的致死性。

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Klebsiella pneumoniae, a worldwide cause of nosocomial infections, is one of the most common causes of death in newborns in nurseries. In this study, we investigated the role of interleukin-1 (IL-1) in an experimental animal model of neonatal sepsis, using a natural antagonist of IL-1 receptors, the IL-1 receptor antagonist (IL-1Ra), to block IL-1's effects in neonatal Klebsiella sepsis in the absence of antibiotic treatment. Newborn Wistar-Kyoto rats were injected intraperitoneally with a single dose (10 mg/kg) of either IL-1Ra (n = 43) or human serum albumin as a control (n = 40). At the same time, a 50% lethal dose of K. pneumoniae was injected subcutaneously. No antibiotics were given at any time. After 10 days, survival was 60% for the albumin group and 80% for the IL-1Ra group (P < 0.01). IL-1Ra treatment also afforded protection when the dose of bacteria was increased sixfold (P < 0.01). There were two episodes of leukopenia in the control group, which were suppressed by IL-1Ra (P < 0.01 and P < 0.001). IL-1 and IL-6 levels were lower in the IL-1Ra-treated group (P < 0.05 and P < 0.001, respectively). No differences between the two groups were observed in the number of bacteria in cultures of the blood, lungs, liver, or spleen. When IL-1Ra (10 mg/kg) was given both at time zero and 24 h after bacterial challenge, lethality was significantly increased (P < 0.01). Single doses of IL-1Ra of from 20 to 40 mg/kg progressively increased lethality compared with controls (P < 0.01) in both Wistar-Kyoto and Sprague-Dawley strain rats. In the same model, low doses of IL-1 itself (0.4 ng per rat), given 24 h prior to bacterial challenge, afforded protection (P < 0.001). These studies suggest that, in the absence of antibiotics, partial blockade of IL-1 receptors improves survival, whereas a longer or greater blockade increases lethality in newborn rats infected with K. pneumoniae.
机译：肺炎克雷伯菌是医院内感染的全球性原因，是托儿所新生儿最常见的死亡原因之一。在这项研究中，我们调查了白介素-1（IL-1）在新生败血症实验动物模型中的作用，该模型使用IL-1受体的天然拮抗剂IL-1受体拮抗剂（IL-1Ra）来阻断在没有抗生素治疗的情况下，IL-1在新生儿克雷伯菌败血症中的作用。向新生Wistar-Kyoto大鼠腹膜内注射单剂量（10 mg / kg）的IL-1Ra（n = 43）或人血清白蛋白作为对照（n = 40）。同时，皮下注射50％致死剂量的肺炎克雷伯菌。任何时候都未给予抗生素。 10天后，白蛋白组的生存率为60％，IL-1Ra组的生存率为80％（P <0.01）。当细菌剂量增加六倍时（P <0.01），IL-1Ra处理也提供了保护。对照组中有2次白细胞减少，被IL-1Ra抑制（P <0.01和P <0.001）。 IL-1Ra治疗组的IL-1和IL-6水平较低（分别为P <0.05和P <0.001）。两组之间在血液，肺，肝或脾脏培养物中的细菌数量没有差异。当在细菌攻击后的零时和24小时都给予IL-1Ra（10 mg / kg）时，致死率显着增加（P <0.01）。在Wistar-Kyoto和Sprague-Dawley应变大鼠中，单剂量的IL-1Ra从20到40 mg / kg都比对照组逐渐增加了致死性（P <0.01）。在同一模型中，在细菌攻击前24小时给予低剂量的IL-1本身（每只大鼠0.4 ng）可提供保护（P <0.001）。这些研究表明，在不使用抗生素的情况下，部分阻断IL-1受体可以提高存活率，而更长或更长时间的阻断作用则可以增加感染肺炎克雷伯菌的新生大鼠的致死率。

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