Current address: Cornel University, New York, NY, USA.
Rheumatoid factor induction in murine models of liver injury
Article first published online: 29 NOV 2006
Clinical & Experimental Immunology
Volume 147, Issue 2, pages 324–329, February 2007
How to Cite
Nowak, U., Gill, K., Skamene, E. and Newkirk, M. M. (2007), Rheumatoid factor induction in murine models of liver injury. Clinical & Experimental Immunology, 147: 324–329. doi: 10.1111/j.1365-2249.2006.03277.x
- Issue published online: 5 JAN 2007
- Article first published online: 29 NOV 2006
- Accepted for publication 3 November 2006
- alcoholic liver disease;
- carbon tetrachloride;
- rheumatoid factor;
- Toll-like receptors
Alcoholic liver disease and hepatitis C are associated with the production of autoantibodies such as rheumatoid factors (RF), which bind to IgG and can aid in host defence, but are also associated with pathological conditions such as rheumatoid arthritis. Because little is known about the role of RF in liver disease, we characterized the RF production that either occurred spontaneously in response to alcohol consumption or was induced by injection of an Escherichia coli glycolipoprotein in C57Bl/6 mice. Whereas severe liver damage was induced by carbon tetrachloride (CCl4), minimal damage was caused by chronic alcohol consumption. Liver damage was monitored by measurements of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Circulating RF was induced in response to chronic alcohol consumption; the latter probably involved Toll-like receptor ligation. In contrast, CCl4-induced damage was not associated with RF induction. However, concurrent treatment with an E. coli glycolipoprotein macromolecule that induced RF, protected against CCL4-induced liver damage as measured by a highly significant decrease (P = 0·008) at 4 weeks in AST and ALT. RF induced by E. coli glycolipoprotein correlated with ‘protection’ from liver damage, indicating that the RF autoimmune response does not necessarily exacerbate liver disease.