A/J mice are resistant while C57BL/6J are susceptible to
casein-induced secondary
amyloidosis. One mechanism responsible for this phenotypic expression of resistance/susceptibility was shown to operate at the level of production of the '
amyloid-enhancing factor' (AEF).
AEF and processing of the
apo-SAA protein appear almost concomitantly during amyloidogenesis. In order to determine if
AEF played a role in the processing of the
apo-SAA protein, three major parameters (apo-SAA1/apo-SAA2 ratios, level of
AEF, and fibril formation) were determined during
casein-induced secondary
amyloidosis. Kinetics of
AEF production and serum levels of the two major
apo-SAA isotypes were compared in A/J and C57BL/6J animals. Both strains showed equal relative amounts of the two isotypes after seven, 15 and 21
casein injections, irrespective of the fact that the A/J strain had no detectable level of
AEF and no
amyloid deposition; while C57BL/6J mice had a high
AEF level and were amyloidotic after 15 and 21
injections. An increased apo-SAA1/apo-SAA2 ratio due to a decrease in apo-SAA2 was noted after 38 days of
casein injections when both strains had extensive deposits of
amyloid fibrils. Involvement of
AEF as an effector molecule was determined by following the ratio of the two major serum
apo-SAA isotypes and fibril formation during an accelerated protocol of
amyloid induction in C57BL/6J animals.
AEF had no direct effect on
apo-SAA isotype ratios in the serum.