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急性弓形虫病期间的肠道病理变化依赖于白细胞介素-4,且与寄生虫负荷无关。

Intestinal pathology during acute toxoplasmosis is IL-4 dependent and unrelated to parasite burden.

作者信息

Nickdel M B, Lyons R E, Roberts F, Brombacher F, Hunter C A, Alexander J, Roberts C W

机构信息

Department of Immunology, Strathclyde Institute for Biomedical Sciences, University of Strathclyde, Glasgow, UK.

出版信息

Parasite Immunol. 2004 Feb;26(2):75-82. doi: 10.1111/j.0141-9838.2004.00686.x.

DOI:10.1111/j.0141-9838.2004.00686.x
PMID:15225294
Abstract

The role of interleukin-4 (IL-4) during the course of Toxoplasma gondii infection was studied using IL-4-/- mice and their wild-type (WT) counterparts on a C57BL/6 background. Following oral infection with T. gondii tissue cysts an exacerbative role for IL-4 was demonstrated and IL-4-/- mice were found to be more resistant to infection than WT mice as measured by significantly reduced mortality. Furthermore pathology in the small intestine was less severe in IL-4-/- mice although conversely liver pathology was greater than in wild-type mice. Significantly, plasma IL-12 and IFN-gamma levels, which peaked at days 6 and 8, respectively, were higher in IL-4-/- mice. The exacerbatory role of IL-4 in the intestine was found by competitive RT-PCR not to be associated with increased parasite burdens but was related to comparative expression of IL-10.

摘要

利用白细胞介素-4(IL-4)基因敲除小鼠及其C57BL/6背景的野生型(WT)对照小鼠,研究了IL-4在刚地弓形虫感染过程中的作用。经口感染刚地弓形虫组织包囊后,证实IL-4具有加重感染的作用,通过显著降低死亡率测定发现,IL-4基因敲除小鼠比野生型小鼠对感染更具抵抗力。此外,IL-4基因敲除小鼠小肠的病理学变化较轻,尽管相反地,其肝脏病理学变化比野生型小鼠更严重。值得注意的是,IL-4基因敲除小鼠血浆中的IL-12和IFN-γ水平分别在第6天和第8天达到峰值,且更高。通过竞争性逆转录聚合酶链反应发现,IL-4在肠道中的加重作用与寄生虫负荷增加无关,而是与IL-10的相对表达有关。

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