Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA.
Virology. 2011 Sep 1;417(2):281-92. doi: 10.1016/j.virol.2011.05.015. Epub 2011 Jul 13.
Biliary atresia (BA) is a progressive fibro-inflammatory pediatric liver disease in which osteopontin (OPN), a glycoprotein with inflammatory and fibrogenic activity, may play a pathogenic role. The current studies were conducted in a mouse model of rotavirus-induced BA to test the hypotheses that live but not inactivated rotavirus causes antigenemia, upregulation of hepatic OPN expression, and induction of BA and fibrosis; and that OPN is necessary for development of BA. Prolonged or transient antigenemia developed in mice inoculated with live or inactivated virus, respectively, but only live virus upregulated hepatic OPN and caused BA and fibrosis. OPN was expressed in intra- and extrahepatic bile ducts in healthy mice and in mice with BA. OPN-deficient mice, similar to WT mice, developed BA. Together, these data show that live but not inactivated rotavirus causes upregulation of hepatic OPN expression and BA but that OPN is not necessary for development of BA.
先天性胆道闭锁（BA）是一种进行性纤维炎症性儿科肝病，骨桥蛋白（OPN）可能在其中发挥致病作用。该研究在轮状病毒诱导的 BA 小鼠模型中进行，旨在验证以下假设：活病毒而非失活病毒引起抗原血症、肝组织 OPN 表达上调以及诱导 BA 和纤维化；OPN 是 BA 发生所必需的。分别接种活病毒和失活病毒的小鼠出现持续或短暂的抗原血症，但只有活病毒上调肝组织 OPN 并导致 BA 和纤维化。OPN 在健康小鼠和 BA 小鼠的肝内外胆管中表达。与 WT 小鼠相似，OPN 缺陷型小鼠也发生 BA。综上所述，这些数据表明，活病毒而非失活病毒引起肝组织 OPN 表达上调和 BA，但 OPN 不是 BA 发生所必需的。
