ABSTRACT
Chronic inflammation is perhaps the most common link between a num ber of liver d iseases/risk factors and development of end-stage cirrhosis and in some cases, cancer. Orthotopic liver transplantation remains the only potential cure for most end-stage liver diseases, given the reservations
concerning use of transgenic organs (Patience et al, 1997), gene therapeutic approaches (Marshall, 2000; Afford and Young, 2001) and the lack of progress with bioartificial liver developm ent (Strain and Neuberger, 2002), However, transplantation is unlikely to be a solution to the problem of inflammatory liver disease on a global scale due to its technical complexity and inadequate supply of donor organs (Krasko
et al, 2003). While the surgical procedures at major liver transplant centres are highly successful, recipients usually require permanent immunosuppression, which has uncertain long-term consequences (Cherikh et al., 2003; Everson et al., 2003; Nash and Gimson, 2003). Thus, if we are to devise more effective therapeutic strategies for the treatm ent or amelioration of end-stage liver disease, there is an urgent need to understand much more about the underlying mechanisms which drive liver inflammatory responses.
