Infection with murine gammaherpesvirus 68 exacerbates inflammatory bowel disease in IL-10-deficient mice

被引:16
|
作者
Nelson, D. A. [1 ]
Petty, C. C. [1 ]
Bost, Kenneth L. [1 ]
机构
[1] Univ N Carolina, Dept Biol, Charlotte, NC 28223 USA
关键词
IL-10; Gammaherpesvirus; Inflammatory bowel disease; Colitis; EPSTEIN-BARR-VIRUS; INTERLEUKIN-10-DEFICIENT MICE; ULCERATIVE-COLITIS; VIRAL BURDEN; CROHNS-DISEASE; DEFICIENT MICE; T-CELLS; MONONUCLEOSIS; PATHOGENESIS; BACTERIA;
D O I
10.1007/s00011-009-0059-x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:881 / 889
页数:9
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