Host immunity and pathogen strain contribute to intestinal disaccharidase impairment following gut infection.
Host immunity and pathogen strain contribute to intestinal disaccharidase impairment following gut infection.
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DOI：
10.4049/jimmunol.1100606
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发表时间：
2011-10-01
期刊：
影响因子：
--
通讯作者：
Singer SM
中科院分区：
文献类型：
--
作者：
Solaymani-Mohammadi S;Singer SM
小肠感染或其他炎症性损伤常导致双糖酶水平降低。利用贾第虫病小鼠模型，我们研究了宿主免疫和病原体毒力在感染后介导双糖酶缺乏中的作用。C57BL/6J小鼠感染人十二指肠贾第虫WB和GS两株。GS菌株感染后，WT小鼠的蔗糖酶、麦芽糖酶和乳糖酶水平下降，而WB菌株感染后则没有下降。CD4缺陷小鼠和SCID小鼠均未能消除感染，且未表现出双糖酶缺乏。β2微球蛋白敲除动物控制的感染与wt型小鼠相似，但双糖酶活性没有下降。对脾脏和肠系膜淋巴结细胞产生细胞因子的分析显示，WB和GS感染后均产生白细胞介素(IL)-4、IL-10、IL-13、IL-17、IL-22、TNF-α和IFN-γ，其中IFN-γ是两种寄生虫菌株的显性细胞因子。与脾细胞相比，在对寄生虫提取物的反应中，肠系膜淋巴结细胞产生的细胞因子水平较低，尽管总体模式相似。这些数据表明，T细胞反应介导寄生虫清除，同时也有助于发病。它们还表明，病原体菌株的差异也可以决定感染的结果，并进一步加深我们对人贾第虫病临床差异的理解。
Infection or other inflammatory insults in the small intestine often result in reduced disaccharidase enzyme levels. Using a mouse model of giardiasis, we examined the role of host immunity and pathogen virulence in mediating disaccharidase deficiency following infection. C57BL/6J mice were infected with two strains, WB and GS, of the human parasite Giardia duodenalis. The levels of sucrase, maltase, and lactase decreased in WT mice after infection with the GS strain but not with the WB strain. Both CD4 deficient and SCID mice failed to eliminate the infection and did not exhibit disaccharidase deficiency. β2microglobulin knockout animals controlled infections similar to WT-type mice but exhibited no decrease in disaccharidase activity. Analysis of cytokine production by spleen and mesenteric lymph node cells showed production of interleukin (IL)-4, IL-10, IL-13, IL-17, IL-22, TNF-α and IFN-γ following infection with both WB and GS, with IFN-γ being the dominant cytokine for both parasite strains. Mesenteric lymph node cells produced lower levels of cytokines compared with splenocytes in responses to parasite extract, although the overall pattern was similar. These data suggest that T cell responses mediate parasite clearance while also contributing to pathogenesis. They also demonstrate that differences in pathogen strain can also determine the outcome of infection and further our understanding of the clinical variation seen in human giardiasis.
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影响因子：
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作者：
Panaro, Maria Antonietta;Cianciulli, Antonia;Cavallo, Pasqua
通讯作者：
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DOI：
10.4269/ajtmh.2009.81.538
发表时间：
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