Secondary amyloidosis was induced in mice with daily consecutive injections of casein or in an accelerated form with the injection of the "Amyloid-Enhancing Factor" (AEF). Innate susceptibility to the disease operated at the level of the production of AEF. AEF activity was purified to one protein component with an apparent molecular weight of 55,100Da. Increased disappearance of the amyloid A (AA) fibril precursor apo-SAA2 did not correlate exactly with amyloid deposition. Multiple splenic macrophage phenotypes and functions were modulated during the two induction protocols. Splenic macrophages from normal or casein-injected mice could not degrade in vitro HDL$ sb3$-SAA2. The catabolism was induced by the exogenous addition of soluble AEF and/or Serum Amyloid P. Finally, AA and amyloid PO proteins were simultaneously deposited in the spleen with respect to time and tissue localization during the two induction protocols. In conclusion, the appearance of AEF in organs during the development of secondary amyloidosis was accompanied by the modulation of the splenic macrophage phenotype and function.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.74542 |
Date | January 1990 |
Creators | Hébert, Lise |
Publisher | McGill University |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | English |
Detected Language | English |
Type | Electronic Thesis or Dissertation |
Format | application/pdf |
Coverage | Doctor of Philosophy (Division of Experimental Medicine.) |
Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
Relation | alephsysno: 001126730, proquestno: AAINN66393, Theses scanned by UMI/ProQuest. |
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