Laboratório de Imunopatologia, Núcleo de Pesquisas em Ciências Biológicas (NUPEB), Universidade Federal de Ouro Preto (UFOP), Ouro Preto, Minas Gerais, Brazil.
PLoS One. 2012;7(3):e32912. doi: 10.1371/journal.pone.0032912. Epub 2012 Mar 7.
Although metacyclic and blood trypomastigotes are completely functional in relation to parasite-host interaction and/or target cell invasion, they differ in the molecules present on the surface. Thus, aspects related to the variability that the forms of T. cruzi interacts with host cells may lead to fundamental implications on the immune response against this parasite and, consequently, the clinical evolution of Chagas disease. We have shown that BT infected mice presented higher levels of parasitemia during all the acute phase of infection. Moreover, the infection with either MT or BT forms resulted in increased levels of total leukocytes, monocytes and lymphocytes, specifically later for MT and earlier for BT. The infection with BT forms presented earlier production of proinflammatory cytokine TNF-α and later of IFN-γ by both T cells subpopulations. This event was accompanied by an early cardiac inflammation with an exacerbation of this process at the end of the acute phase. On the other hand, infection with MT forms result in an early production of IFN-γ, with subsequent control in the production of this cytokine by IL-10, which provided to these animals an immunomodulatory profile in the end of the acute phase. These results are in agreement with what was found for cardiac inflammation where animals infected with MT forms showed intense cardiac inflammation later at infection, with a decrease in the same at the end of this phase. In summary, our findings emphasize the importance of taking into account the inoculums source of T. cruzi, since vectorial or transfusional routes of T. cruzi infection may trigger distinct parasite-host interactions during the acute phase that may influence relevant biological aspects of chronic Chagas disease.
虽然循环和血内变形体在寄生虫-宿主相互作用和/或靶细胞入侵方面完全具有功能，但它们在表面存在的分子上有所不同。因此，与 T. cruzi 与宿主细胞相互作用的变异性相关的方面可能对针对这种寄生虫的免疫反应产生根本影响，进而对恰加斯病的临床演变产生影响。我们已经表明，BT 感染的小鼠在整个急性感染期间的寄生虫血症水平更高。此外，无论是 MT 还是 BT 形式的感染都会导致总白细胞、单核细胞和淋巴细胞水平升高，具体来说，MT 形式的感染会导致升高更早，BT 形式的感染则会导致升高更晚。BT 形式的感染会更早地产生促炎细胞因子 TNF-α，随后两种 T 细胞亚群会产生 IFN-γ。这一事件伴随着早期的心脏炎症，在急性阶段结束时，这一过程加剧。另一方面，MT 形式的感染会导致 IFN-γ 的早期产生，随后通过 IL-10 控制这种细胞因子的产生，这为这些动物在急性阶段结束时提供了一种免疫调节表型。这些结果与心脏炎症的结果一致，感染 MT 形式的动物在感染后期表现出强烈的心脏炎症，而在该阶段结束时则减少。总之，我们的研究结果强调了考虑 T. cruzi 接种物来源的重要性，因为 T. cruzi 的媒介或输血途径的感染可能在急性阶段引发不同的寄生虫-宿主相互作用，从而影响慢性恰加斯病的相关生物学方面。
