Play it, Jen

Every good movie has a piano player somewhere in the background--
sometimes seen, usually unseen.
Seldom really noticed.
The feeling, the very soul of a scene, is created by that person tinkering at the keys.
It has been said, "All the world's a stage."
Well then...Play it, Jen.

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Location: Over Yonder, Missouri

I'm a California Native transplanted to the Missouri Ozarks. I've learned how to chase cows in high heels and load hay faster than you can say "Coco Chanel." These are some of our pictures and stories of living in a land with breath-taking beauty and adventure around every bend.

Sunday, August 20, 2006

Type-I but not type-II interferon receptor knockout mice are susceptible to biliary atresia.

Entrez PubMed
Department of Pediatric Surgery, Medical School Hannover, 30625 Hannover, Germany.

The etiology of biliary atresia (BA) is not yet understood, but recent studies have shown inflammation with an up-regulated interferon (IFN) activity in the intra- and extrahepatic bile ducts of patients with BA. These findings support an inflammatory/infectious cause of BA as mimicked in our infective murine model. To study the role of the IFN receptors in our model, we used mice with inactivated INF-alpha/beta receptor A129, with inactivated IFN-gamma receptor G129, or inactivation of both interferon receptors AG129 as well as the wild type controls W129. Mice were infected with rotavirus within 48h of birth and 7 d postpartum. The incidence of BA in each group was determined during a 3 wk period. In the second week the virus load was measured. BA incidence was 76% in A129 and 67% in AG129 animals, whereas in the G129 group only 33% of the pups developed BA. The wild type presented with a BA-incidence of 15%, while 7 d old mice failed to develop BA. There was no significant difference in the virus load of the livers between the groups independent of clinical symptoms. In conclusion, inactivation of type I INF-receptor significantly increases the incidence of BA following postpartal rotavirus infection. This effect is independent of the presence of type II-INF-receptors. Thus, in our model a type I IFN-linked deregulation of the innate immune system appears to be crucial for the induction of biliary atresia.

PMID: 16641200 [PubMed - indexed for MEDLINE]


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