Oral infection of C57BL/6 mice with Toxoplasma gondii:: A new model of inflammatory bowel disease?

Oral infection of C57BL/6 mice with Toxoplasma gondii:: A new model of inflammatory bowel disease?
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DOI:
10.1086/338006
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发表时间:
2002-02-15
影响因子:
6.4
通讯作者:
Liesenfeld, O
Liesenfeld, O
中科院分区:
医学2区
文献类型:
--
作者:
Liesenfeld, O

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弓形虫感染是通过口服途径自然获得的,通过摄入含有寄生虫包囊的未煮熟或生肉,或通过摄入受污染的水或受包囊或卵囊污染的食物。经口感染100个T. C57 BL/6小鼠在感染后13天内死亡,而BALB/c小鼠存活。在感染第7天,在C57 BL/6小鼠中观察到回肠中绒毛和粘膜细胞的大量坏死,但在BALB/c小鼠中未观察到。CD 4(+)T细胞、干扰素-γ、肿瘤坏死因子-α和诱导型一氧化氮合酶介导坏死的发展。这些发现表明Th 1型免疫病理学,寄生虫复制似乎参与了感染的前3天。关于炎症性肠病免疫发病机制的小鼠和人类研究(E。例如,在一个实施例中,克罗恩病)也表明Th 1型免疫病理学。结果表明,小鼠经口感染T.本文讨论了炎性肠病的弓形虫和鼠模型。
Infection with Toxoplasma gondii is naturally acquired through the oral route by ingestion of undercooked or raw meat containing cysts of the parasite or through ingestion of contaminated water or food contaminated with cysts or oocysts. Following peroral infection with 100 cysts of the ME49 strain of T. gondii, C57BL/6 mice die within 13 days after infection, whereas BALB/c mice survive. At day 7 of infection, massive necrosis of the villi and mucosal cells in the ilea is observed in C57BL/6 but not BALB/c mice. CD4(+) T cells, interferon-gamma, tumor necrosis factor-alpha, and inducible nitric oxide synthase mediate the development of necrosis. These findings indicate a Th1-type immunopathology, with parasite replication appearing to be involved in the first 3 days of infection. Murine and human studies on the immunopathogenesis of inflammatory bowel disease (e. g., Crohn's disease) also indicate a Th1-type immunopathology. The shared and distinct features of oral infection of mice with T. gondii and murine models of inflammatory bowel disease are discussed herein.