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首页> 外文期刊>Comparative Medicine >Lack of Effect of Murine Astrovirus Infection on Dextran Sulfate-induced Colitis in NLRP3-deficient Mice
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Lack of Effect of Murine Astrovirus Infection on Dextran Sulfate-induced Colitis in NLRP3-deficient Mice

机译：小鼠缺乏鼠血管病毒感染在NLRP3缺陷小鼠中对硫酸葡聚糖诱导的结肠炎的影响

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Murine astrovirus (MuAstV) is a recently identified, widespread infection among laboratory mice. MuAstV is found predominantly in the gastrointestinal tract of mice. Human and turkey astroviruses have been shown to disrupt tight junctions in the intestinal epithelium. The potential of MuAstV to alter research results was tested in a well-established dextran sodium sulfate (DSS)-induced colitis model in Nod-like receptor 3 (NLRP3)-deficient mice. This model offers a direct approach to determine whether MuAstV, as a component of the mouse microbiome, contributes to the issue of poor reproducibility in murine inflammatory bowel disease research. In this model, defective inflammasome activation causes loss of epithelial integrity, resulting in leakage of intestinal bacteria and colitis. Our goal was to determine whether MuAstV, which also may affect intestinal permeability, altered the onset or severity of colitis. Male and female mice (age, 8 to 12 wk) homozygous or heterozygous for an NLRP3 mutation were inoculated orally with MuAstV or mock-inoculated with media 3 or 20 d prior to being exposed to 2% DSS in their drinking water for 9 d. MuAstV infection alone did not cause clinical signs or histopathologic changes in NLRP3(-/-) or NLRP3(+/-) mice. No significant difference was seen in weight loss, clinical disease, intestinal inflammation, edema, hyperplasia, or mucosal ulceration between MuAstV-infected and mock-infected mice that received 2% DSS for 9 d. Therefore, MuAstV does not appear to be a confounding variable in the DSS colitis model in NLRP3 mice.
机译：鼠星病毒（Muastv）是最近发现的，在实验室小鼠中普遍存在的感染。 muastv主要在小鼠的胃肠道中发现。已被证明人和土耳其星形病毒在肠上皮中破坏紧密连接。 Muastv改变研究结果的潜力在结核良好的葡聚糖硫酸钠（DSS）诱导的Nod样受体3（NLRP3） - 缺少小鼠中进行了测试。该模型提供了一种直接的方法来确定Muastv是否作为小鼠微生物组的组分，有助于鼠炎症肠病研究的不良再现性问题。在该模型中，有缺陷的炎症激活导致上皮完整性的丧失，导致肠道细菌和结肠炎的泄漏。我们的目标是确定Muastv是否可能影响肠道渗透性，改变结肠炎的发病或严重程度。对于NLRP3突变的雄性和雌性小鼠（年龄，8至12WK）纯合或杂合，用muastv或用培养基3或20d在其饮用水中暴露于2％DS的培养基3或20d，以进行9天。单独的Muastv感染没有引起NLRP3（ - / - ）或NLRP3（+/-）小鼠的临床症状或组织病理学变化。在减肥，临床疾病，肠炎，水肿，增生剂或受影响2％DSS的MUASTV感染和嘲弄的小鼠之间没有显着差异。因此，Muastv在NLRP3小鼠中似乎在DSS结肠炎模型中似乎是一种混淆变量。

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