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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Effect of Antiflagellar Human Monoclonal Antibody on Gut-Derived Pseudomonas aeruginosa Sepsis in Mice
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Effect of Antiflagellar Human Monoclonal Antibody on Gut-Derived Pseudomonas aeruginosa Sepsis in Mice

机译：抗鞭毛人单克隆抗体对小鼠肠源性铜绿假单胞菌败血症的影响

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We evaluated the effect of antiflagellar human monoclonal antibody on gut-derived Pseudomonas aeruginosa sepsis. Mice were given a suspension of P. aeruginosa SP10052 in their drinking water and were simultaneously treated with ampicillin (200 mg/kg of body weight) to disrupt the normal bacterial flora. Cyclophosphamide was then administered to induce leukopenia and translocation of the P. aeruginosa that had colonized the gastrointestinal tract, thereby producing gut-derived generalized sepsis. In this model, intraperitoneal injection of 100 μg of antiflagellar human monoclonal antibody (SC-1225) per mouse for 5 consecutive days significantly (P < 0.01) increased the survival rate compared with that for mice treated with bovine serum albumin (BSA). Treatment with SC-1225 significantly reduced the average number of viable bacteria in portal blood, liver, and heart blood compared with the average number after treatment with BSA. Furthermore, the presence in serum of the inflammatory cytokines tumor necrosis factor alpha and interleukin 6 were evaluated as markers of severity of infection, and the results showed that the levels of these cytokines in mice treated with SC-1225 were significantly decreased in comparison with those in BSA-treated control mice. Although there was no significant difference in the number of bacteria that colonized the intestine, SC-1225 treatment significantly increased bacterial opsonophagocytosis by cultured peritoneal macrophages from mice with or without cyclophosphamide pretreatment. Our results indicate that antiflagellar human monoclonal antibody SC-1225 protects mice against gut-derived sepsis caused by P. aeruginosa and suggest that such an effect is due to its opsonophagocytic activity and the reduced motility of the translocated bacteria once the bacteria move from the intestine into the bloodstream.
机译：我们评估了抗鞭毛人单克隆抗体对肠源性铜绿假单胞菌败血症的作用。给小鼠悬浮 P。饮用水中的铜绿SP10052并同时用氨苄西林（200 mg / kg体重）处理以破坏正常细菌菌群。然后施用环磷酰胺以诱导白细胞减少和 P的易位。铜绿假单胞菌已经定居在胃肠道，从而产生了肠道衍生的广义败血症。在该模型中，与用牛治疗的小鼠相比，每只小鼠连续5天腹腔注射100μg抗鞭毛人单克隆抗体（SC-1225）可以显着提高存活率（ P <0.01）血清白蛋白（BSA）。与用BSA处理后的平均数相比，用SC-1225处理可显着减少门静脉血，肝和心脏血液中平均活菌数。此外，评估血清中炎性细胞因子肿瘤坏死因子α和白介素6的存在作为感染严重程度的标志，结果表明，与SC-1225处理的小鼠相比，这些细胞因子的水平显着降低在BSA处理的对照小鼠中。尽管在肠道中定植的细菌数量没有显着差异，但是SC-1225处理可显着增加来自培养小鼠腹膜巨噬细胞的细菌调理吞噬作用，而小鼠的腹膜巨噬细胞可进行或不进行环磷酰胺预处理。我们的结果表明，抗鞭毛人单克隆抗体SC-1225保护小鼠免受 P引起的肠道源性败血症的侵害。铜绿假单胞菌并提示这种作用是由于其调理吞噬作用，以及一旦细菌从肠道进入血流而降低了易位细菌的运动能力。

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