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无囊包旋毛虫(Trichinella spp.)、T. papuae 减轻了 DSS 诱导的小鼠结肠炎的严重程度。

Non-encapsulated Trichinella spp., T. papuae, diminishes severity of DSS-induced colitis in mice.

机构信息

Department of Helminthology, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.

出版信息

Asian Pac J Allergy Immunol. 2013 Jun;31(2):106-14. doi: 10.12932/AP0238.31.2.2013.

DOI:10.12932/AP0238.31.2.2013
PMID:23859409
Abstract

BACKGROUND

Helminths use various mechanisms to avoid host immunity and protect themselves from being eliminated. Despite evading host immune responses, immunosuppression and regulation mechanisms elicit functions that diminish the adverse effects of unrelated inflammatory diseases.

OBJECTIVE

We investigated whether helminthic infections can ameliorate inflammatory diseases.

METHODS

Mice were infected with Trichinella papuae and then subjected to induced colitis through the oral administration of dextran sulfate sodium (DSS). Macroscopic and microscopic examinations measured weight loss, stool consistency, gross bleeding, colon length, and tissue inflammation. In addition, cytokine expression was observed in colon tissue by SYBR real-time RT-PCR to investigate the Th1, Th2, and regulatory cytokines.

RESULT

The results showed that T. papuae infection decreased the severity of DSS-inducedcolitis, including weight loss, bloody diarrhea, shortening of colon, and colon tissue damage in mice (p <0.05). The expression level of IL-4 was high in the colons of DSS-treated mice without helminthic infection, while infected mice with DSS treatment had lower IL-4 levels (p <0.05). Uninfected DSS-treated mice failed to produce IL-10 mRNA in colon tissue, which may cause more severe colitis. In contrast, prior T. papuae infection DSS-treated mice had IL-10 levels in the colon significant lower than the normal and infected control groups.

CONCLUSION

Our data provide the evidence that prior T. papuae infection can ameliorate DSS-induced colitis in mice and may be considered for a novel therapeutic strategy against immunological diseases in the future.

摘要

背景

寄生虫利用各种机制来避免宿主免疫并保护自己免受消除。尽管逃避宿主免疫反应,但免疫抑制和调节机制引发的功能可减轻无关炎症性疾病的不良影响。

目的

我们研究了寄生虫感染是否可以改善炎症性疾病。

方法

用旋毛虫感染小鼠,然后通过口服葡聚糖硫酸钠(DSS)诱导结肠炎。通过体重减轻、粪便稠度、肉眼可见出血、结肠长度和组织炎症的宏观和微观检查来衡量。此外,通过 SYBR 实时 RT-PCR 观察结肠组织中细胞因子的表达,以研究 Th1、Th2 和调节性细胞因子。

结果

结果表明,旋毛虫感染可降低 DSS 诱导的结肠炎的严重程度,包括体重减轻、血性腹泻、结肠缩短和组织损伤(p<0.05)。在未感染寄生虫的 DSS 处理小鼠的结肠中,IL-4 的表达水平较高,而感染 DSS 的寄生虫处理的小鼠的 IL-4 水平较低(p<0.05)。未感染 DSS 处理的小鼠在结肠组织中未能产生 IL-10 mRNA,这可能导致更严重的结肠炎。相比之下,先前的旋毛虫感染 DSS 处理的小鼠的结肠中 IL-10 水平明显低于正常和感染对照组。

结论

我们的数据提供了证据表明,先前的旋毛虫感染可以改善 DSS 诱导的小鼠结肠炎,并且可能在未来被考虑作为一种针对免疫性疾病的新型治疗策略。

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