Department of Biology, University of North Carolina at Charlotte, 28223, USA.
Inflamm Res. 2009 Dec;58(12):881-9. doi: 10.1007/s00011-009-0059-x. Epub 2009 Jun 21.
We questioned whether infection with murine gammaherpesvirus 68 (HV-68) might exacerbate inflammatory bowel disease using mice deficient in IL-10 (IL-10-/-) as a model of developing colitis.
Groups of C57BL/6 mice and IL-10-/- mice were mock-treated or infected with HV-68. Two months following infection, mice were euthanized and a variety of parameters were measured to quantify the extent of inflammation and the presence of virus. Measurements included survival, body weight, splenomegaly, colonic disease scores, liver histopathology, viable bacteria in the liver, and splenic viral burden.
IL-10-/- mice infected with HV-68 displayed reduced survival, lower body weights, increased splenomegaly, exacerbated colonic disease scores, increased numbers of viable bacteria in the liver, and increased leukocyte liver infiltration when compared to mock-treated IL-10-/- mice or HV-68 infected C57BL/6 mice. Surprisingly, levels of infectious or latent virus were not significantly different between the groups of mice exposed to HV-68.
The presence of HV-68 in IL-10-/- mice exacerbates the developing clinical disease in this animal model of colitis.
我们通过 IL-10 缺陷（IL-10-/-）小鼠模型来研究感染鼠γ疱疹病毒 68（HV-68）是否会加剧炎症性肠病，以此来提出疑问。
将 C57BL/6 小鼠和 IL-10-/- 小鼠分为模拟治疗组和感染组，并感染 HV-68。感染两个月后，处死小鼠并测量多种参数以量化炎症程度和病毒存在情况。测量内容包括生存率、体重、脾肿大、结肠疾病评分、肝脏组织病理学、肝脏中存活细菌数量和脾脏病毒载量。
与模拟治疗的 IL-10-/- 小鼠或感染 HV-68 的 C57BL/6 小鼠相比，感染 HV-68 的 IL-10-/- 小鼠的生存率降低，体重减轻，脾肿大加剧，结肠疾病评分升高，肝脏中存活细菌数量增加，白细胞浸润肝脏。令人惊讶的是，暴露于 HV-68 的各组小鼠之间的传染性或潜伏病毒水平没有明显差异。
IL-10-/- 小鼠中 HV-68 的存在会加剧这种结肠炎动物模型中正在发展的临床疾病。
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