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Strongyloides venezuelensis-infection alters the profile of cytokines and liver inflammation in mice co-infected with Schistosoma mansoni
Cytokine ( IF 3.8 ) Pub Date : 2020-03-01 , DOI: 10.1016/j.cyto.2019.154931
Michelle Carvalho de Rezende 1 , João Marcelo Peixoto Moreira 1 , Laura Liana Maggi Fernandes 1 , Vanessa Fernandes Rodrigues 1 , Deborah Negrão-Corrêa 1
Affiliation  

Human co-infection by helminth species is frequent, but their consequences are mostly unknown. Here, we investigate the impact of Strongyloides venezuelensis co-infection on the immune response, schistosome burden, and the associated pathology of schistosomiasis in mice. Co-infection did not alter the schistosome parasite burden, but reduced the IL-4/IL-10 ratio during acute schistosomiasis, indicating induction of modulatory mechanisms. Simultaneous infection with S. venezuelensis and S. mansoni increased the liver concentration of IFN-γ and altered the Th2/Th1 balance, leading to great infiltration of neutrophils and macrophages, which resulted in larger liver inflammation and increased serum transaminase activity in comparison with mono-infected mice. Mice infected with S. venezuelensis at two and four weeks after S. mansoni infection showed significant increase of Th1/Th2/Th17/Treg cytokines and strong cellular infiltration in the liver in comparison with mono-infected mice. However, only in mice co-infected after two weeks of schistosomiasis, the liver immune response leads to more intense Th2 polarization, increased liver inflammation, and transaminase serum activity. S. venezuelensis co-infection during chronic schistosomiasis did not significantly alter liver inflammation. Therefore, S. venezuelensis co-infection affects the host immune responses and morbidity of schistosomiasis, but the effects largely depend on the stage of the S. mansoni infection.

中文翻译:

委内瑞拉圆线虫感染改变了曼氏血吸虫共感染小鼠的细胞因子和肝脏炎症的特征

蠕虫物种的人类共同感染很常见,但其后果大多未知。在这里,我们研究了委内瑞拉圆线虫共感染对小鼠免疫反应、血吸虫负担和血吸虫病相关病理学的影响。合并感染并没有改变血吸虫寄生虫的负担,但在急性血吸虫病期间降低了 IL-4/IL-10 的比率,表明调节机制的诱导。同时感染 S. venezuelensis 和 S. mansoni 会增加肝脏 IFN-γ 浓度,改变 Th2/Th1 平衡,导致中性粒细胞和巨噬细胞大量浸润,导致肝脏炎症更大,血清转氨酶活性高于单- 感染小鼠。在 S. venezuelensis 感染后 2 周和 4 周的小鼠。与单一感染的小鼠相比,mansoni 感染显示出 Th1/Th2/Th17/Treg 细胞因子显着增加和肝脏细胞浸润强烈。然而,仅在血吸虫病两周后共同感染的小鼠中,肝脏免疫反应导致更强烈的 Th2 极化、肝脏炎症增加和转氨酶血清活性。慢性血吸虫病期间的 S. venezuelensis 合并感染并未显着改变肝脏炎症。因此,S. venezuelensis 合并感染会影响宿主免疫反应和血吸虫病的发病率,但其影响很大程度上取决于 S. mansoni 感染的阶段。肝脏免疫反应导致更强烈的 Th2 极化,增加肝脏炎症和转氨酶血清活性。慢性血吸虫病期间的 S. venezuelensis 合并感染并未显着改变肝脏炎症。因此,S. venezuelensis 合并感染会影响宿主免疫反应和血吸虫病的发病率,但其影响很大程度上取决于 S. mansoni 感染的阶段。肝脏免疫反应导致更强烈的 Th2 极化,增加肝脏炎症和转氨酶血清活性。慢性血吸虫病期间的 S. venezuelensis 合并感染并未显着改变肝脏炎症。因此,S. venezuelensis 合并感染会影响宿主免疫反应和血吸虫病的发病率,但其影响很大程度上取决于 S. mansoni 感染的阶段。
更新日期:2020-03-01
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