Abstract：
Trypanosoma cruzi is a parasite with a high capacity to adapt to the host. Animal models have already demonstrated that the tropism of this parasite occurs not only in cardiac/digestive tissues but also in adipose tissue (AT). That said, the consequences ofT. cruziinfection for AT and the implications of treatment with Benzonidazole in this tissue are under discussion. Here, we tested the hypothesis that T. cruzi infection in adipose tissue upon treatment with Benzonidazole (Bz) and the interaction of mononuclear immune cells (PBMC) influences the relative expression of ACAT1, FASN, and PNPLA2 genes. Thus, stem cells derived from adipose tissue (ADSC) after adipogenic differentiation were indirectly cultivated with PBMC after infection with the T. cruzi Y strain and treatment with Bz. We use the TcSAT-IAM system and RT-qPCR to evaluate the parasite load and the relative quantification (ΔCt) of the ACAT1, FASN, and PNPLA2 genes. Our results demonstrate that treatment with Bz did not reduce adipocyte infection in the presence (p-value: 0.5796) or absence (p-value: 0.1854) of cultivation with PBMC. In addition, even though there is no statistical difference when compared to the control group (AT), T. cruzi induces the FASN expression (Rq: 14.00). However, treatment with Bz in AT suggests the increases of PNPLA2 expression levels (Rq: 12.58), even in the absence of T. cruzi infection. During indirect cultivation with PBMC, T. cruzi smooths the expression of PNPLA2 (Rq: 0.824) and instigates the expression of ACAT1 (Rq: 1.632) and FASN (Rq: 1.394). Furthermore, the treatment with Bz during infection induces PNPLA2 expression (Rq: 1.871), maintaining FASN expression levels (Rq: 1.334). Given this, our results indicate that treatment with Benzonidazole did not decrease T. cruzi infection in adipose tissue. However, treating the adipocyte cells with Bz during the interaction with PBMC cells influences the lipid pathways scenario, inducing lipolytic metabolism through the expression of PNPLA2.
摘要：
克氏锥虫是一种具有高度适应宿主能力的寄生虫。动物模型已经证明，这种寄生虫的嗜性不仅发生在心脏/消化组织中，也发生在脂肪组织（AT）中。那就是说,T的后果。正在讨论AT的Cruzi感染以及在该组织中使用苯并硝唑治疗的意义。这里,我们检验了用苯并硝唑（Bz）处理的脂肪组织中的克氏锥虫感染和单核免疫细胞（PBMC）的相互作用影响ACAT1，FASN，和PNPLA2基因。因此，在用T.cruziY菌株感染并用Bz处理后，用PBMC间接培养成脂分化后的脂肪组织（ADSC）干细胞。我们使用TcSAT-IAM系统和RT-qPCR来评估寄生虫负载和ACAT1，FASN的相对定量（ΔCt），和PNPLA2基因。我们的结果表明，在存在（p值：0.5796）或不存在（p值：0.1854）PBMC培养的情况下，用Bz处理均未减少脂肪细胞感染。此外,即使与对照组（AT）相比没有统计学差异，克氏杆菌诱导FASN表达(Rq:14.00)。然而,在AT中用Bz治疗表明PNPLA2表达水平增加（Rq：12.58），即使没有克氏杆菌感染。在用PBMC间接培养期间，克氏杆菌平滑PNPLA2(Rq:0.824)的表达并激发ACAT1(Rq:1.632)和FASN(Rq:1.394)的表达。此外，感染期间用BZ处理诱导PNPLA2表达（Rq：1.871），维持FASN表达水平(Rq:1.334)。鉴于此,我们的结果表明，苯并硝唑治疗并不能减少脂肪组织中的克氏锥虫感染。然而,在与PBMC细胞相互作用期间用Bz处理脂肪细胞会影响脂质途径方案，通过PNPLA2的表达诱导脂肪分解代谢。
