Leishmaniasis is a group of infectious diseases caused by protozoa of the genus and its immunopathogenesis results from an unbalanced immune response during the infection. Diabetes is a chronic disease resulting from dysfunction of the body's production of insulin or the ability to use it properly, leading to hyperglycemia causing tissue damage and impairing the immune system. The objective of this work was to evaluate the effects of hyperglycemia and diabetes during infection and how these conditions alter the immune response to the parasite. An hyperglycemic stimulus model using THP-1-derived macrophages and an experimental diabetes with streptozotocin (STZ) in C57BL/6 mice was employed to investigate the impact of diabetes and hyperglicemia in infection. We observed that hyperglycemia impair the leishmanicidal capacity of macrophages derived from THP-1 cells and reverse the resistance profile that C57BL/6 mice have against infection by , inducing more exacerbated lesions compared to non-diabetic animals. In addition, the hyperglycemic stimulus favored the increase of markers related to the phenotype of M2 macrophages. The induction of experimental diabetes in C57BL/6 mice resulted in a failure in the production of nitric oxide (NO) in the face of infection and macrophages from diabetic animals failed to process and present Leishmania antigens, being unable to activate and induce proliferation of antigen-specific lymphocytes. Together, these data demonstrate that diabetes and hyperglycemia can impair the cellular immune response, mainly of macrophages, against infection by parasites of the genus Leishmania.

中文翻译：

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亚马逊利什曼原虫感染调节高血糖和糖尿病中的氧化应激，损害巨噬细胞的功能和免疫反应

利什曼病是由该属原虫引起的一组传染病，其免疫发病机制是感染过程中免疫反应失衡所致。糖尿病是一种慢性疾病，是由于身体产生胰岛素或无法正确使用胰岛素的能力出现障碍而导致的，导致高血糖，从而导致组织损伤并损害免疫系统。这项工作的目的是评估感染期间高血糖和糖尿病的影响，以及这些条件如何改变对寄生虫的免疫反应。采用 THP-1 衍生巨噬细胞和 C57BL/6 小鼠实验性糖尿病链脲佐菌素 (STZ) 的高血糖刺激模型来研究糖尿病和高血糖对感染的影响。我们观察到，高血糖会损害 THP-1 细胞衍生的巨噬细胞的杀利什曼细胞能力，并逆转 C57BL/6 小鼠对感染的抵抗力，与非糖尿病动物相比，诱导更严重的病变。此外，高血糖刺激有利于与 M2 巨噬细胞表型相关的标记物的增加。C57BL/6小鼠实验性糖尿病的诱导导致面对感染时一氧化氮（NO）的产生失败，并且糖尿病动物的巨噬细胞无法处理和呈递利什曼原虫抗原，无法激活和诱导抗原增殖-特异性淋巴细胞。总之，这些数据表明，糖尿病和高血糖会损害细胞免疫反应，主要是巨噬细胞针对利什曼原虫属寄生虫感染的免疫反应。