Expression of a biologically active recombinant mouse IL-1 receptor antagonist and its use in vivo to modulate aspects of the acute phase response.

摘要: Recombinant mouse IL-1receptor antagonist protein (rmIL-1ra) was expressed in Escherichia coli. In vivo administration of rmIL-1ra, a casein-induced murine model acute inflammation, completely abolished the hepatic induction mRNAs specifying serum amyloid A1 (A-SAA1) and A-SAA2 for up to 12 h, indicating that A-SAA mRNA synthesis is totally IL-1 driven. protein, however, present rmIL-1ra-treated casein-stimulated mice (although at lower levels than untreated mice) h extrahepatic driven part by factors acting independently IL-1. Hepatic other phase reactants (APRs), P component, C-reactive alpha1-acid glycoprotein, C3 were also induced with casein after as SAP C3. These inductions only partially inhibited expression latter APRs (unlike A-SAA) partly negative apolipoprotein A-I albumin down-regulated stimulation. rmIL-1ra restored but not apo levels, differential regulation these APRs. The will be useful studies IL-1-mediated gene models inflammation.