皮肤利什曼病（CL）是一种被忽视的热带皮肤病，由原生动物寄生虫利什曼原虫引起。在埃塞俄比亚，CL 主要由埃塞俄比亚利什曼原虫引起，可以有不同的临床形式。本研究的目的是评估这些不同的形式是否与寄生虫遗传和宿主系统免疫特征的差异相关。在这里，我们分析了 48 种临床寄生虫分离株的全基因组序列数据以及来自 CL 患者队列的系统免疫特征，他们于 2019 年 1 月至 2022 年 1 月在埃塞俄比亚北部 Nefas Mewcha 招募。我们的结果表明，根据全基因组相似性的排列测试，在单一埃塞俄比亚环境中具有不同表现的 CL 病例的寄生虫来自相同的遗传群体。此外，全基因组关联的逻辑回归测试没有发现任何与疾病表现显着相关的个体遗传变异。我们还测量了 129 名患有不同形式 CL 的 CL 患者的血浆趋化因子和细胞因子水平。趋化因子 [eotaxin、eotaxin-3、白细胞介素 (IL)-8、干扰素 (IFN)-γ 诱导蛋白-10 (IP-10)、单核细胞趋化蛋白 (MCP)-1、MCP-4、巨噬细胞-衍生趋化因子 (MDC)、巨噬细胞炎症蛋白 (MIP)-1α、MIP-1β 以及胸腺和激活调节趋化因子 (TARC)] 或细胞因子（IFN-γ、IL-1β、白介素-2、IL-4、IL）通过 Kruskal-Wallis 检验测量，不同临床表现的 CL 中测得的 -6、IL-10、IL-12p70、IL-13、肿瘤坏死因子-α）水平显着不同。我们还将这些患者与健康的非地方病对照进行了比较：我们的结果显示 CL 患者存在趋化因子（IP-10、MCP-1、MCP-4、MDC、MIP-1α、MIP-1β 和 TARC），但没有细胞因子免疫特征，如与通过 Mann-Whitney 测试测量的健康非地方性对照相比。我们的研究结果没有发现与 CL 不同临床表现相关的全身免疫特征或寄生虫遗传因素。© 2024。作者。

Cutaneous leishmaniasis (CL) is a neglected tropical skin disease, caused by the protozoan parasite Leishmania. In Ethiopia, CL is mainly caused by Leishmania aethiopica and can present in different clinical forms. The aim of this study was to assess whether these different forms are associated with differences in parasite genetic and host systemic immune signatures.Here we analysed the whole genome sequence data for 48 clinical parasite isolates and the systemic immune signature from a cohort of CL patients, who were recruited in Nefas Mewcha, Northern Ethiopia, from January 2019 to January 2022.Our results show that parasites from CL cases with different presentations in a single Ethiopian setting are from the same genetic population based on a permutation test of genome-wide similarity. Furthermore, a logistic regression test for genome wide association did not identify any individual genetic variants significantly associated with disease presentation. We also measured plasma chemokine and cytokine levels of 129 CL patients presenting with different forms of CL. None of the chemokine [eotaxin, eotaxin-3, interleukin (IL)-8, interferon (IFN)-γ-induced protein-10 (IP-10), monocyte chemoattractant protein (MCP)-1, MCP-4, macrophage-derived chemokines (MDC), macrophage inflammatory protein (MIP)-1α, MIP-1β and thymus- and activation-regulated chemokine (TARC)] or cytokine (IFN-γ, IL-1β, interleukin-2, IL-4, IL-6, IL-10, IL-12p70, IL-13, tumor necrosis factor-α) levels measured were significantly different between the different clinical presentations of CL, as measured by Kruskal-Wallis test. We also compared those with healthy nonendemic controls: our results show a chemokine (IP-10, MCP-1, MCP-4, MDC, MIP-1α, MIP-1β and TARC) but not a cytokine immune signature in patients with CL as compared to healthy nonendemic controls, as measured by Mann-Whitney test.The results of our study did not identify a systemic immune signature or parasite genetic factors associated with different clinical presentation of CL.© 2024. The Author(s).