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Wuchereria bancrofti macrophage migration inhibitory factor-2 (rWbaMIF-2) ameliorates experimental colitis.
Parasite Immunology ( IF 1.4 ) Pub Date : 2020-02-06 , DOI: 10.1111/pim.12698
Shriram Ramani 1 , Nikhil Chauhan 1 , Vishal Khatri 1 , Connie Vitali 2 , Ramaswamy Kalyanasundaram 1
Affiliation  

Immunomodulatory molecules produced by helminth parasites are receiving much attention recently as novel therapeutic agents for inflammation and autoimmune diseases. In this study, we show that macrophage migration inhibitory factor (MIF) homologue from the filarial parasite, Wuchereria bancrofti (rWbaMIF-2), can suppress inflammation in a dextran sulphate sodium salt (DSS)-induced colitis model. The disease activity index (DAI) in DSS given mice showed loss of body weight and bloody diarrhoea. At autopsy, colon of these mice showed severe inflammation and reduced length. Administration of rWbaMIF-2 significantly reduced the DAI in DSS-induced colitis mice. rWbaMIF-2-treated mice had no blood in the stools, and their colon length was similar to the normal colon with minimal inflammation and histological changes. Pro-inflammatory cytokine genes (TNF-α, IL-6, IFN-γ, IL-1β, IL-17A and NOS2) were downregulated in the colon tissue and peritoneal macrophages of rWbaMIF-2-treated mice. However, there were significant increases in IL-10-producing Treg and B1 cells in the colon and peritoneal cavity of rWbaMIF-2-treated mice. These findings suggested that rWbaMIF-2 treatment significantly ameliorated the clinical symptoms, inflammation and colon pathology in DSS given mice. This immunomodulatory effect of rWbaMIF-2 appeared to be by promoting the infiltration of Treg cells into the colon.

中文翻译:

Wuchereria bancrofti巨噬细胞迁移抑制因子2(rWbaMIF-2)可改善实验性结肠炎。

由蠕虫寄生虫产生的免疫调节分子作为炎症和自身免疫疾病的新型治疗剂最近受到了广泛关注。在这项研究中,我们表明来自丝状寄生虫Wuchereria bancrofti(rWbaMIF-2)的巨噬细胞迁移抑制因子(MIF)同源物可以抑制葡聚糖硫酸盐(DSS)诱导的结肠炎模型的炎症。给予DSS的小鼠的疾病活动指数(DAI)显示体重减轻和血性腹泻。尸检时,这些小鼠的结肠显示出严重的炎症并减少了长度。施用rWbaMIF-2可显着降低DSS诱导的结肠炎小鼠的DAI。用rWbaMIF-2处理的小鼠的粪便中没有血液,并且其结肠长度与正常结肠相似,并且炎症和组织学变化极小。在rWbaMIF-2处理的小鼠的结肠组织和腹膜巨噬细胞中,促炎性细胞因子基因(TNF-α,IL-6,IFN-γ,IL-1β,IL-17A和NOS2)下调。但是,rWbaMIF-2处理的小鼠结肠和腹膜腔中产生IL-10的Treg和B1细胞显着增加。这些发现表明,rWbaMIF-2治疗显着改善了给予DSS的小鼠的临床症状,炎症和结肠病理。rWbaMIF-2的这种免疫调节作用似乎是通过促进Treg细胞向结肠的浸润来实现的。这些发现表明,rWbaMIF-2治疗显着改善了给予DSS的小鼠的临床症状,炎症和结肠病理。rWbaMIF-2的这种免疫调节作用似乎是通过促进Treg细胞向结肠的浸润来实现的。这些发现表明,rWbaMIF-2治疗显着改善了给予DSS的小鼠的临床症状,炎症和结肠病理。rWbaMIF-2的这种免疫调节作用似乎是通过促进Treg细胞向结肠的浸润来实现的。
更新日期:2020-03-27
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