Leishmania braziliensis is the main causative agent of American tegumentary leishmaniasis in Brazil. Current treatment includes different drugs that have important side effects and identification of cases of parasite resistance to treatment support the search for new therapeutic strategies. Recent findings have indicated that CXCL10, a chemokine that recruits and activates Th1 cells, NK cells, macrophages, dendritic cells and B lymphocytes, is a potential alternative to treat Leishmania infection. Here, we tested CXCL10 immunotherapy against experimental infection caused by an antimony‐resistant isolate of Leishmania braziliensis. Following infection, mice were treated with CXCL10 for 7 days after onset of lesions. We demonstrate that mice treated with CXCL10 controlled lesion progression and parasite burden more efficiently comparing to controls. An increased IFN‐γ, IL‐10, TGF‐β and low IL‐4 production combined with a distinct inflammatory infiltrate composed by activated macrophages, lymphocytes and granulomas was observed in the CXCL10‐treated group comparing to controls. However, CXCL10 and Glucantime combined therapy did not improve CXCL10‐induced protective effect. Our findings reinforce the potential of CXCL10 immunotherapy as an alternative treatment against infection caused by L. braziliensis resistant to conventional chemotherapy.

中文翻译：

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CXCL10免疫调节作用对巴西利什曼原虫的难治性锑分离株引起的感染

巴西利什曼原虫是巴西美洲被膜性利什曼原虫病的主要病原体。当前的治疗方法包括具有重要副作用的不同药物，对寄生虫的抗药性病例的鉴定有助于寻找新的治疗策略。最近的发现表明，CXCL10是一种募集并激活Th1细胞，NK细胞，巨噬细胞，树突状细胞和B淋巴细胞的趋化因子，是治疗利什曼原虫感染的潜在选择。在这里，我们测试了针对巴西利什曼原虫抗药性分离株引起的实验性感染的CXCL10免疫疗法。感染后，在病变发作后用CXCL10治疗小鼠7天。我们证明，与对照相比，用CXCL10治疗的小鼠可更有效地控制病变进程和寄生虫负担。与对照组相比，在CXCL10处理组中观察到IFN-γ，IL-10，TGF-β的增加和低IL-4的产生，以及由活化的巨噬细胞，淋巴细胞和肉芽肿组成的明显炎症浸润。但是，CXCL10和葡聚糖联合疗法不能改善CXCL10诱导的保护作用。我们的发现增强了CXCL10免疫疗法作为对抗由传统化学疗法抗药的巴西乳杆菌引起的感染的替代疗法的潜力。