Department of Pharmacology, Institute of Postgraduate Medical Education and Research, Kolkata, India.
Cancer Biology and Inflammatory Disorder Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology, Kolkata, India.
Parasite Immunol. 2021 Jan;43(1):e12783. doi: 10.1111/pim.12783. Epub 2020 Aug 27.
Leishmania donovani, the causative agent for visceral leishmaniasis (VL), modulates host monocytes/macrophages to ensure its survival. However, knowledge regarding the host-parasite interactions underpinning the disease remains limited. As disease progression is associated with polarization of monocytes/macrophages towards M2, which is regulated by cytokines IL-4/IL-13 and IL-10, this study evaluated the status of key IL-4- and IL-10 driven markers in experimental models of VL, as also evaluated their correlation, if any, with parasite load.
In liver and splenic tissues from L donovani-infected hamsters and BALB/c mice, the parasite burden was determined along with mRNA expression of IL-4-driven markers, that is CD206, Arginase-I, CCL17, CCL22, PPAR-γ, STAT6, KLF4, FIZZ1 and YM1 along with IL-10-driven markers, CXCL13, IL-10, TGF-β, VDR, CCR2 and CYP27A1.
The mRNA expression of IL-4- and IL-10-driven markers was enhanced in both models, but only in the hamster model, the splenic tissues demonstrated a positive correlation between all the IL-10-driven markers and parasite load.
Contrary to human VL, both models demonstrated an increased expression of IL-4- and IL-10-driven markers.
利什曼原虫（Leishmania donovani）是内脏利什曼病（VL）的病原体，它可调节宿主单核细胞/巨噬细胞以确保其存活。然而，与疾病相关的宿主-寄生虫相互作用的知识仍然有限。由于疾病的进展与单核细胞/巨噬细胞向 M2 极化有关，而 M2 是由细胞因子 IL-4/IL-13 和 IL-10 调节的，因此本研究评估了在 VL 的实验模型中关键的 IL-4 和 IL-10 驱动标志物的状态，并评估了它们与寄生虫负荷的任何相关性。
在感染利什曼原虫的仓鼠和 BALB/c 小鼠的肝和脾组织中，测定寄生虫负荷以及 IL-4 驱动标志物的 mRNA 表达，即 CD206、精氨酸酶-I、CCL17、CCL22、PPAR-γ、STAT6、KLF4、FIZZ1 和 YM1，以及 IL-10 驱动标志物，即 CXCL13、IL-10、TGF-β、VDR、CCR2 和 CYP27A1。
两种模型中 IL-4 和 IL-10 驱动标志物的 mRNA 表达均增强，但仅在仓鼠模型中，脾组织中所有 IL-10 驱动标志物与寄生虫负荷之间存在正相关。
与人类 VL 相反，两种模型均表现出 IL-4 和 IL-10 驱动标志物的表达增加。
