Núcleo de Pesquisas em Ciências Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, Brazil.
Trop Med Int Health. 2013 Apr;18(4):466-76. doi: 10.1111/tmi.12071. Epub 2013 Feb 12.
Chagas heart disease is developed as a result of the infection with Trypanosoma cruzi. Protein malnutrition contributes to secondary immunodeficiency. The aim of this study was to investigate the role of a low protein diet on the production of endothelin-1 and CX3CL1 in blood and cardiac tissue samples in an experimental model with T. cruzi infection.
Fisher rats were submitted to low protein (6%) and normal protein (15%) diets and then infected with the Y strain of T. cruzi. At days 15 and 120, parasites and immune cells were evaluated.
The low protein diet reduced body weight and circulating serum proteins, but promoted elevation of CX3CL1 and endothelin-1 levels in infected animals, which were unable to control blood parasitemia replication. In heart tissue, the low protein diet reduced cardiac CX3CL1, endothelin-1 and leucocyte infiltration in the acute phase, in particular CD68 and CD163 macrophage phenotypes.
Together, these results highlight the participation of endothelin-1 and CX3CL1 in the inflammatory process of Chagas diesease, both being mediators partially controlled by the host nutritional status.
克氏锥虫感染可导致克氏心脏病。蛋白质营养不良可导致继发性免疫缺陷。本研究旨在探讨低蛋白饮食对克氏锥虫感染实验模型中血液和心脏组织样本中内皮素-1 和 CX3CL1 产生的影响。
将费希尔大鼠分为低蛋白(6%)和正常蛋白(15%)饮食组,并感染 Y 株克氏锥虫。在第 15 天和第 120 天,评估寄生虫和免疫细胞。
低蛋白饮食降低了体重和循环血清蛋白水平,但促进了感染动物中 CX3CL1 和内皮素-1 水平的升高,这些动物无法控制血液寄生虫血症的复制。在心脏组织中,低蛋白饮食降低了急性期心脏 CX3CL1、内皮素-1 和白细胞浸润,特别是 CD68 和 CD163 巨噬细胞表型。
综上所述,这些结果强调了内皮素-1 和 CX3CL1 参与了克氏病的炎症过程,两者都是宿主营养状况部分控制的介质。