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A mathematical model of murine macrophage infected with Leishmania sp

机译:利什曼原虫感染的小鼠巨噬细胞的数学模型

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Infection by Leishmania can cause diseases ranging from self-healing cutaneous to visceral dissemination that can lead to death if untreated. In order to explore the early phase of the infection and the role of macrophages, we implement a system of differential equations involving the major players in the innate immune response to leishmaniasis (i.e., parasites in the intracellular and free form, infected and uninfected macrophages, and NO/ROS). The model was adjusted and validated using data from C57BL/6, KO and SCID mice published in the literature. The key findings were the surprisingly more active macrophages in the mice knockouts for IL-12 and IFN-g. This result can be interpreted as an indication of an M2b polarization of the macrophages in these mice. Sensitivity Analysis shows that NO/ROS secretion rate is more important to Leishmania control then the mechanisms of killing intracellular parasites. This model is a useful tool for comprehending the infection and treatments.
机译:利什曼原虫感染可引起多种疾病,从皮肤的自我修复到内脏的扩散,如果不及时治疗,可能导致死亡。为了探索感染的早期阶段和巨噬细胞的作用,我们实施了一个微分方程系统,涉及对利什曼病的先天免疫反应的主要参与者(即,细胞内和游离形式的寄生虫,感染和未感染的巨噬细胞,和NO / ROS)。使用文献中发表的C57BL / 6,KO和SCID小鼠的数据对模型进行调整和验证。关键发现是在敲除IL-12和IFN-g的小鼠中令人惊讶地更具活性的巨噬细胞。该结果可以解释为这些小鼠中巨噬细胞的M2b极化的指示。敏感性分析表明,NO / ROS的分泌速率对控制利什曼原虫的危害比杀灭细胞内寄生虫的机理更为重要。该模型是理解感染和治疗的有用工具。

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