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Latex proteins downregulate inflammation and restores blood-coagulation homeostasis in acute Salmonella infection
Memórias do Instituto Oswaldo Cruz ( IF 2.5 ) Pub Date : 2020-11-23 , DOI: 10.1590/0074-02760200458
Brandon Ferraz Sousa 1 , Ayrles Fernanda Brandão da Silva 1 , José Vitor Lima-Filho 2 , Anderson Gomes Agostinho 1 , Denise Nunes Oliveira 3 , Nylane Maria Nunes de Alencar 1 , Cleverson Diniz Teixeira de Freitas 1 , Márcio Viana Ramos 1
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BACKGROUND Calotropis procera latex protein fraction (LP) was previously shown to protect animals from septic shock. Further investigations showed that LP modulate nitric oxide and cytokines levels. OBJECTIVES To evaluate whether the protective effects of LP, against lethal bacterial infection, is observed in its subfractions (LPPII and LPPIII). METHODS Subfractions (5 and 10 mg/kg) were tested by i.p. administration, 24 h before challenging with lethal injection (i.p.) of Salmonella Typhimurium. LPPIII (5 mg/kg) which showed higher survival rate was assayed to evaluate bacterial clearance, histopathology, leukocyte recruitment, plasma coagulation time, cytokines and NO levels. FINDINGS LPPIII protected 70% of animals of death. The animals given LPPIII exhibited reduced bacterial load in blood and peritoneal fluid after 24 h compared to the control. LPPIII promoted macrophage infiltration in spleen and liver. LPPIII restored the coagulation time of infected animals, increased IL-10 and reduced NO in blood. MAIN CONCLUSIONS LPPIII recruited macrophages to the target organs of bacterial infection. This addressed inflammatory stimulus seems to reduce bacterial colonisation in spleen and liver, down regulate bacterial spread and contribute to avoid septic shock.

中文翻译:

乳胶蛋白可下调炎症,并恢复急性沙门氏菌感染的凝血稳态

背景技术先前已证明嗜钙麦芽菌乳胶蛋白级分(LP)可保护动物免于败血症性休克。进一步的研究表明,LP调节一氧化氮和细胞因子水平。目的评估在其亚组分(LPPII和LPPIII)中是否观察到了LP对致命细菌感染的保护作用。方法致死性注射鼠伤寒沙门氏菌攻击前24小时,通过腹膜内注射分别检测5和10 mg / kg的亚组分。检测显示较高存活率的LPPIII(5 mg / kg),以评估细菌清除率,组织病理学,白细胞募集,血浆凝固时间,细胞因子和NO水平。研究结果LPPIII保护了70%的死亡动物。与对照组相比,给予LPPIII的动物在24小时后血液和腹膜液中细菌含量降低。LPPIII促进脾脏和肝脏中的巨噬细胞浸润。LPPIII恢复了感染动物的凝血时间,增加了IL-10并降低了血液中的NO。主要结论LPPIII将巨噬细胞募集到细菌感染的靶器官。该针对性的炎症刺激似乎减少了脾脏和肝脏中的细菌定植,下调了细菌的传播并有助于避免败血性休克。
更新日期:2020-11-23
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