Murase Letícia Sayuri, de Souza João Vítor Perez, de Lima Neto Quirino Alves, de Mello Tatiane França Perles, Cardoso Bruna Muller, Lera-Nonose Daniele Stéfanie Sara Lopes, Teixeira Jorge Juarez Vieira, Lonardoni Maria Valdrinez Campana, Demarchi Izabel Galhardo
Graduation in Biomedicine, Department of Clinical Analysis and Biomedicine,State University of Maringá,Maringá, PR,Brazil.
Department of Biochemistry,State University of Maringá,PR,Brazil.
Parasitology. 2018 Oct;145(12):1499-1509. doi: 10.1017/S0031182018000367. Epub 2018 Mar 13.
This is a systematic review on the role of metalloproteases in the pathogenicity of the American tegumentary leishmaniasis (ATL) caused by New World Leishmania species. The review followed the PRISMA method, searching for articles in PubMed, EMBASE, LILACS and ISI Web of Science, by employing the following terms: 'leishmaniasis', 'cutaneous leishmaniasis', 'mucocutaneous leishmaniasis', 'diffuse cutaneous leishmaniasis', 'Leishmania' and 'metalloproteases'. GP63 of New World Leishmania species is a parasite metalloproteases involved in the degradation and cleavage of many biological molecules as kappa-B nuclear factor, fibronectin, tyrosine phosphatases. GP63 is capable of inhibiting the activity of the complement system and reduces the host's immune functions, allowing the survival of the parasite and its dissemination. High serological/tissue levels of host matrix metalloproteases (MMP)-9 have been associated with tissue damage during the infection, while high transcriptional levels of MMP-2 related with a satisfactory response to treatment. Host MMPs serological and tissue levels have been investigated using Western Blot, zymography, and Real Time polymerase chain reaction. GP63 detection characterizes species and virulence in promastigotes isolated from lesions samples using techniques mentioned previously. The monitoring of host MMPs levels and GP63 in Leishmania isolated from host samples could be used on the laboratory routine to predict the prognostic and treatment efficacy of ATL.
这是一篇关于金属蛋白酶在由新大陆利什曼原虫引起的美洲皮肤利什曼病(ATL)致病性中作用的系统综述。该综述遵循PRISMA方法,通过使用以下术语在PubMed、EMBASE、LILACS和ISI科学网中搜索文章:“利什曼病”、“皮肤利什曼病”、“黏膜皮肤利什曼病”、“弥漫性皮肤利什曼病”、“利什曼原虫”和“金属蛋白酶”。新大陆利什曼原虫的GP63是一种寄生虫金属蛋白酶,参与许多生物分子如κ-B核因子、纤连蛋白、酪氨酸磷酸酶的降解和裂解。GP63能够抑制补体系统的活性并降低宿主的免疫功能,从而使寄生虫得以存活并传播。宿主基质金属蛋白酶(MMP)-9的高血清学/组织水平与感染期间的组织损伤有关,而MMP-2的高转录水平与对治疗的满意反应有关。已使用蛋白质免疫印迹法、酶谱法和实时聚合酶链反应研究了宿主MMPs的血清学和组织水平。使用上述技术对从病变样本中分离的前鞭毛体进行GP63检测可鉴定物种和毒力。监测从宿主样本中分离的利什曼原虫中的宿主MMPs水平和GP63可用于实验室常规操作,以预测ATL的预后和治疗效果。