肿瘤坏死因子受体p55缺陷对C57BL/6小鼠感染亚马逊利什曼原虫（利什曼原虫属）易感性的影响。

Impact of tumor necrosis factor receptor p55 deficiency in susceptibility of C57BL/6 mice to infection with Leishmania (Leishmania) amazonensis.

作者信息

Cargnelutti Diego Esteban, Salomón María Cristina, Celedon Verónica, Cuello-Carrión Fernando Darío, Gea Susana, Di Genaro María Silvia, Scodeller Eduardo Alberto

机构信息

Instituto de Medicina y Biología Experimental de Cuyo (IMBECU), CCT-Mendoza, CONICET, Argentina; Área de Parasitología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza, Argentina.

Área de Parasitología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza, Argentina.

出版信息

J Microbiol Immunol Infect. 2016 Apr;49(2):271-5. doi: 10.1016/j.jmii.2014.03.009. Epub 2014 May 22.

DOI:10.1016/j.jmii.2014.03.009

PMID:24856420

Abstract

Tumor necrosis factor (TNF) is involved in host resistance to several intracellular pathogens. Although the critical role of TNF receptor (TNFR)p55 in Leishmania (Leishmania) major infection has been demonstrated, the impact of TNFRp55 deficiency on L. (L.) amazonensis infection has not been explored. L. (L.) amazonensis-infected TNFRp55(-/-) mice failed to resolve lesions, whereas C57BL/6 wild-type mice completely healed. The susceptibility of the TNFRp55(-/-) mice was characterized by higher lesion size and histopathological damage in comparison with the wild-type mice. A marked increased of the splenic index was observed in the TNFRp55(-/-) mice after 15 weeks infection. These results show that in the absence of TNFRp55, L. (L.) amazonensis-infected knockout mice fail to resolve lesions, whereas wild-type mice completely heal.

摘要

肿瘤坏死因子（TNF）参与宿主对多种细胞内病原体的抵抗。尽管已证明TNF受体（TNFR）p55在硕大利什曼原虫（利什曼原虫属）感染中起关键作用，但TNFRp55缺陷对亚马逊利什曼原虫（L. (L.) amazonensis）感染的影响尚未得到研究。感染亚马逊利什曼原虫的TNFRp55（-/-）小鼠无法消除病变，而C57BL/6野生型小鼠则完全愈合。与野生型小鼠相比，TNFRp55（-/-）小鼠的易感性表现为病变面积更大和组织病理学损伤更严重。感染15周后，TNFRp55（-/-）小鼠的脾脏指数显著增加。这些结果表明，在缺乏TNFRp55的情况下，感染亚马逊利什曼原虫的基因敲除小鼠无法消除病变，而野生型小鼠则完全愈合。