Induction of the acute-phase serum protein SAA requires both RNA and protein synthesis.
SAA is a normal acute-phase serum protein which has been identified by its cross-reaction with antibodies to the amyloid A fibril protein, AA, that is associated with secondary amyloidosis. The induction of SAA by bacterial lipopolysaccharide (LPS) has been studied with 3 inhibitors of protein synthesis: cycloheximide, actinomycin D, and galactosamine. Each of the 3 agents when administered simultaneously with LPS completely abolishes induction of SAA for at least 6 h. They are all significantly effective when given 1.5 h after LPS but 3 h after LPS the inhibitory effect of actinomycin D on SAA induction is markedly reduced. Cycloheximide alone can also induce significant concentration of SAA, but a longer time is required than for LPS. Thus it appears that the acute-phase SAA response is characterized by both RNA and protein synthesis which is initiated by the acute-phase inducing agent and which precedes the appearance of elevated SAA concentrations in the serum.
D000682:Amyloid / Q000096:biosynthesis / Q000276:immunology; D000818:Animals; D000942:Antigens, Bacterial / Q000008:administration & dosage; D001798:Blood Proteins / Q000096:biosynthesis / Q000276:immunology*; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D005260:Female; D005688:Galactosamine / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000276:immunology; D051379:Mice; D014176:Protein Biosynthesis; D012313:RNA / Q000096:biosynthesis*
D000682:Amyloid; D000942:Antigens, Bacterial; D001798:Blood Proteins; D008070:Lipopolysaccharides; D003609:Dactinomycin; D012313:RNA; D005688:Galactosamine; D003513:Cycloheximide