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Future Microbiol. 2015;10(8):1339-53. doi: 10.2217/FMB.15.54. Epub 2015 Aug 3.
2
Evaluation of mucositis induced by irinotecan after microbial colonization in germ-free mice.无菌小鼠微生物定植后伊立替康诱导的粘膜炎评估。
Microbiology (Reading). 2015 Oct;161(10):1950-1960. doi: 10.1099/mic.0.000149. Epub 2015 Jul 28.
3
Neutrophilic infiltration in lungs of mice with peritonitis in acid or basic medium.酸性或碱性介质中腹膜炎小鼠肺部的中性粒细胞浸润
Int J Clin Exp Med. 2015 Apr 15;8(4):5812-7. eCollection 2015.
4
Pathological changes in acute experimental toxoplasmosis with Toxoplasma gondii strains obtained from human cases of congenital disease.从先天性疾病人类病例中获取的弓形虫菌株所致急性实验性弓形虫病的病理变化。
Exp Parasitol. 2015 Sep;156:87-94. doi: 10.1016/j.exppara.2015.06.002. Epub 2015 Jun 10.
5
The gut microbiota influences blood-brain barrier permeability in mice.肠道微生物群影响小鼠血脑屏障的通透性。
Sci Transl Med. 2014 Nov 19;6(263):263ra158. doi: 10.1126/scitranslmed.3009759.
6
Comparing the effects of acute alcohol consumption in germ-free and conventional mice: the role of the gut microbiota.比较急性酒精摄入在无菌小鼠和常规小鼠中的作用:肠道微生物群的作用。
BMC Microbiol. 2014 Sep 16;14:240. doi: 10.1186/s12866-014-0240-4.
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L-arginine supplementation prevents increases in intestinal permeability and bacterial translocation in male Swiss mice subjected to physical exercise under environmental heat stress.补充精氨酸可预防雄性瑞士小鼠在环境热应激下进行体力活动时肠道通透性和细菌易位的增加。
J Nutr. 2014 Feb;144(2):218-23. doi: 10.3945/jn.113.183186. Epub 2013 Nov 20.
8
Heme oxygenase-1 activity is involved in the control of Toxoplasma gondii infection in the lung of BALB/c and C57BL/6 and in the small intestine of C57BL/6 mice.血红素加氧酶-1 的活性参与 BALB/c 和 C57BL/6 小鼠肺部以及 C57BL/6 小鼠小肠内弓形虫感染的调控。
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Inhibition of tissue inflammation and bacterial translocation as one of the protective mechanisms of Saccharomyces boulardii against Salmonella infection in mice.布拉氏酵母菌抑制组织炎症和细菌易位,作为其抵抗鼠伤寒沙门氏菌感染的保护机制之一。
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本土微生物群对常规和无菌小鼠实验性弓形虫病的影响。

Influence of indigenous microbiota on experimental toxoplasmosis in conventional and germ-free mice.

作者信息

Nascimento Bruna B, Cartelle Christiane T, Noviello Maria de L, Pinheiro Breno V, de Almeida Vitor Ricardo W, Souza Danielle da G, de Vasconcelos Generoso Simone, Cardoso Valbert N, Martins Flaviano Dos S, Nicoli Jacques R, Arantes Rosa M E

机构信息

Departamento de Patologia Geral, Laboratório de Neuro-Imunopatologia Experimental (NIPE), Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.

Departamento de Parasitologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.

出版信息

Int J Exp Pathol. 2017 Aug;98(4):191-202. doi: 10.1111/iep.12236. Epub 2017 Sep 11.

DOI:10.1111/iep.12236
PMID:28895246
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5639263/
Abstract

Toxoplasmosis represents one of the most common zoonoses worldwide. Its agent, Toxoplasma gondii, causes a severe innate pro-inflammatory response. The indigenous intestinal microbiota promotes host animal homoeostasis and may protect the host against pathogens. Germ-free (GF) animals provide an important tool for the study of interactions between host and microbiota. In this study, we assessed the role of indigenous microorganisms in disease development utilizing a murine toxoplasmosis model, which includes conventional (CV) and GF NIH Swiss mice. CV and GF mice orally inoculated with T. gondii had similar survival curves. However, disease developed differently in the two animal groups. In CV mice, intestinal permeability increased and levels of intestinal pro-inflammatory cytokines were altered. In GF animals, there were discrete epithelial degenerative changes and mucosal oedema, but the liver and lungs displayed significant lesions. We conclude that, despite similar survival curves, CV animals succumb to an exaggerated inflammatory response, whereas GF mice fail to produce an adequate systemic response.

摘要

弓形虫病是全球最常见的人畜共患病之一。其病原体刚地弓形虫会引发严重的先天性促炎反应。肠道内的原生微生物群可促进宿主动物的体内平衡,并可能保护宿主抵御病原体。无菌(GF)动物为研究宿主与微生物群之间的相互作用提供了重要工具。在本研究中,我们利用鼠弓形虫病模型评估了原生微生物在疾病发展中的作用,该模型包括常规(CV)和GF NIH瑞士小鼠。经口接种刚地弓形虫的CV和GF小鼠具有相似的生存曲线。然而,两种动物组中的疾病发展情况有所不同。在CV小鼠中,肠道通透性增加,肠道促炎细胞因子水平发生改变。在GF动物中,出现了离散的上皮退行性变化和粘膜水肿,但肝脏和肺部显示出明显病变。我们得出结论,尽管生存曲线相似,但CV动物死于过度的炎症反应,而GF小鼠则未能产生足够的全身反应。