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首页> 外文期刊>Infection and immunity >Both Hemolytic Anemia and Malaria Parasite-Specific Factors Increase Susceptibility to Nontyphoidal Salmonella enterica Serovar Typhimurium Infection in Mice
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Both Hemolytic Anemia and Malaria Parasite-Specific Factors Increase Susceptibility to Nontyphoidal Salmonella enterica Serovar Typhimurium Infection in Mice

机译：溶血性贫血和疟原虫特有的因素都增加了对小鼠非伤寒沙门氏菌血清鼠伤寒感染的敏感性。

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Severe pediatric malaria is an important risk factor for developing disseminated infections with nontyphoidal Salmonella serotypes (NTS). While recent animal studies on this subject are lacking, early work suggests that an increased risk for developing systemic NTS infection during malaria is caused by hemolytic anemia, which leads to reduced macrophage microbicidal activity. Here we established a model for oral Salmonella enterica serotype Typhimurium challenge in mice infected with Plasmodium yoelii nigeriensis. Initial characterization of this model showed that 5 days after coinoculation, P. yoelii nigeriensis infection increased the recovery of S. Typhimurium from liver and spleen by approximately 1,000-fold. The increased bacterial burden could be only partially recapitulated by antibody-mediated hemolysis, which increased the recovery of S. Typhimurium from liver and spleen by 10-fold. These data suggested that both hemolysis and P. yoelii nigeriensis-specific factors contributed to the increased susceptibility to S. Typhimurium. The mechanism by which hemolysis impaired resistance to S. Typhimurium was further investigated. In vitro, S. Typhimurium was recovered 24 h after infection of hemophagocytic macrophages in 2-fold-higher numbers than after infection of mock-treated macrophages, making it unlikely that reduced macrophage microbicidal activity was solely responsible for hemolysis-induced immunosuppression during malaria. Infection with P. yoelii nigeriensis, but not antibody-mediated hemolysis, reduced serum levels of interleukin-12p70 (IL-12p70) in response to S. Typhimurium challenge. Collectively, studies establishing a mouse model for this coinfection suggest that multiple distinct malaria-induced immune defects contribute to increased susceptibility to S. Typhimurium.
机译：严重的儿科疟疾是发展非伤寒沙门氏菌血清型（NTS）传播感染的重要危险因素。尽管缺乏有关该主题的最新动物研究，但早期工作表明，溶血性贫血可导致疟疾在系统性NTS感染中发展的风险增加，从而导致巨噬细胞杀微生物活性降低。在这里，我们建立了感染约氏疟原虫的小鼠口服沙门氏菌血清型鼠伤寒沙门氏菌攻击的模型。该模型的最初特征显示，共接种5天后，黑约氏假单胞菌感染使鼠伤寒沙门氏菌从肝脏和脾脏的回收率提高了约1000倍。抗体介导的溶血仅能部分概括增加的细菌负担，从而使鼠伤寒沙门氏菌从肝脏和脾脏的回收率提高了10倍。这些数据表明溶血和约氏疟原虫特异因子均导致鼠伤寒沙门氏菌的敏感性增加。进一步研究了溶血削弱对鼠伤寒沙门氏菌抗性的机制。在体外，鼠伤寒沙门氏菌在感染了噬菌体巨噬细胞后24小时恢复了2倍，高于感染模拟处理的巨噬细胞感染后的2倍，因此降低的巨噬细胞杀微生物活性不太可能是疟疾中溶血诱导的免疫抑制的唯一原因。用鼠疫沙门氏菌感染，但不进行抗体介导的溶血，可降低鼠伤寒沙门氏菌攻击后的血清白细胞介素12p70（IL-12p70）水平。集体地，建立这种共感染的小鼠模型的研究表明，多种不同的疟疾诱导的免疫缺陷导致对鼠伤寒沙门氏菌的敏感性增加。

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