ABSTRACT
This chapter aims to develop an experimental model of AA amyloidosis that involves C57BL/6 mice with casein (C)-induced amyloidosis and tried to enhance it by injections of dextran sulphate (DS), fibrin (F), and ubiquitin (Ub). It demonstrates that besides the casein which may be capable of forming amyloid fibrils, other inflammatory substances such as F and Ub can enhance its deposition in C57BL/6 mice. F split products and fibrinopeptides also are the factors which enhance the permeability of the blood vessels and chemotaxis of the polymorphonuclear cells. The formation of AA amylod fibril deposits is not well-understood but in the murine model of amyloidosis, deposits increase and are variable in respect to their extent and localization. Amyloidosis is a protein metabolism disorder where normally soluble proteins are transformed into insoluble fibrillar structures, which are deposited in the extracellular space of organs and tissues, thereby resulting in clinical disease.
