与亚马逊利什曼原虫相比，IL-32γ可促进巴西利什曼原虫感染引起的小鼠皮肤损伤的愈合。

IL-32γ promotes the healing of murine cutaneous lesions caused by Leishmania braziliensis infection in contrast to Leishmania amazonensis.

作者信息

Gomes Rodrigo Saar, Silva Muriel Vilela Teodoro, Dos Santos Jéssica Cristina, de Lima Silva Lucas Luiz, Batista Aline Carvalho, Machado Juliana Reis, Teixeira Mauro Martins, Dorta Miriam Leandro, de Oliveira Milton Adriano Pelli, Dinarello Charles A, Joosten Leo A B, Ribeiro-Dias Fátima

机构信息

Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, Brazil.

Department of Internal Medicine and Radboud Center of Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, The Netherlands.

出版信息

Parasit Vectors. 2017 Jul 14;10(1):336. doi: 10.1186/s13071-017-2268-4.

DOI:10.1186/s13071-017-2268-4

PMID:28709468

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5513196/

Abstract

BACKGROUND

Interleukin 32 (IL-32) is a pro-inflammatory cytokine induced in patients with American tegumentary leishmaniasis (ATL) caused by Leishmania braziliensis. Here, we investigated whether IL-32 is also expressed in patient lesions caused by L. amazonensis. In addition, we evaluated experimental L. amazonensis and L. braziliensis infections in C57BL/6 transgenic mice for human IL-32γ (IL-32γTg) in comparison with wild-type (WT) mice that do not express the IL-32 gene.

RESULTS

Human cutaneous lesions caused by L. amazonensis express higher levels of IL-32 than healthy control skin. In mice, the presence of IL-32γ promoted the control of cutaneous lesions caused by L. braziliensis, but not lesions caused by L. amazonensis in an ear dermis infection model. In addition, IL-32γTg mice displayed less tissue parasitism and inflammation in IL-32γTg than WT mice during the healing phase of L. braziliensis infection. Production of antigen-specific pro-inflammatory cytokines was higher in IL-32γTg mice than in WT mice during L. braziliensis infection but not during L. amazonensis infection.

CONCLUSIONS

Human cutaneous lesions caused by L. amazonensis express high levels of IL-32. In mice, the presence of IL-32γ contributes to the lesion healing caused by L. braziliensis but not by L. amazonensis. Data suggest that despite the ability for both species to induce IL-32 in humans, the connections between this cytokine and other immune players induced by related species of parasites can lead to distinct outcomes of the murine infections.

摘要

背景

白细胞介素32（IL-32）是一种促炎细胞因子，在由巴西利什曼原虫引起的美洲皮肤利什曼病（ATL）患者中诱导产生。在此，我们研究了IL-32是否也在由亚马逊利什曼原虫引起的患者病变中表达。此外，我们评估了C57BL/6转基因小鼠（人IL-32γ（IL-32γTg））与不表达IL-32基因的野生型（WT）小鼠相比，感染亚马逊利什曼原虫和巴西利什曼原虫的实验情况。

结果

由亚马逊利什曼原虫引起的人类皮肤病变比健康对照皮肤表达更高水平的IL-32。在小鼠中，在耳部真皮感染模型中，IL-32γ的存在促进了对巴西利什曼原虫引起的皮肤病变的控制，但对亚马逊利什曼原虫引起的病变无效。此外，在巴西利什曼原虫感染的愈合阶段，IL-32γTg小鼠比WT小鼠在IL-32γ中表现出更少的组织寄生和炎症。在巴西利什曼原虫感染期间，IL-32γTg小鼠中抗原特异性促炎细胞因子的产生高于WT小鼠，但在亚马逊利什曼原虫感染期间则不然。

结论

由亚马逊利什曼原虫引起的人类皮肤病变表达高水平的IL-32。在小鼠中，IL-32γ的存在有助于巴西利什曼原虫引起的病变愈合，但对亚马逊利什曼原虫引起的病变无效。数据表明，尽管这两种物种都有能力在人类中诱导IL-32，但这种细胞因子与相关寄生虫物种诱导的其他免疫参与者之间的联系可能导致小鼠感染的不同结果。