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Amyloid‐Enhancing Factor: Production and Response in Amyloidosis‐Susceptible and ‐Resistant Mouse Strains
Author(s) -
Gervais Francine,
Hébert Lise,
Skamene Emil
Publication year - 1988
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.43.4.311
Subject(s) - amyloidosis , biology , inbred strain , aa amyloidosis , amyloid (mycology) , ratón , immunology , endocrinology , pathology , disease , medicine , gene , genetics , familial mediterranean fever , botany
Genetic variations in the development of casein‐induced amyloidosis exist among inbred strains of mice: CBA/J and C57BL/6J mice are susceptible, while A/J strain mice are resistant to this disease. Amyloidosis is usually induced by daily injections of an inflammatory stimulus for 2‐3 wk. The deposition of amyloid in experimental animals can be accelerated by injection of a material called amyloid‐enhancing factor (AEF); when injected concomitantly with an inflammatory stimulus, AEF provokes appearance of amyloidosis as early as 2 days after injection. AEF is extracted from amyloid laden or from normal organs (although in small amount). Our studies were designed to determine if the resistance to amyloidosis seen in A/J mice was either due to a lack of AEF production or to an inability of these mice to respond to AEF. A standard source of CBA/J‐derived AEF facilitated the development of amyloidosis in the organs of both the susceptible (CBA/J, C57BL/6J) and the resistant A/J mice. On the contrary, amyloidosis was only induced in susceptible CBA/J hosts when material derived from susceptible (CBA/J, C57BL/6J) animals was injected. CBA/J mice injected with A/J‐derived AEF preparation did not develop amyloidosis. These results thus suggest that the determination of resistance or susceptibility to secondary amyloidosis could operate at the level of AEF production.