Amyloid enhancing factor and dietary transmission in accelerated amyloid A amyloidosis.
The etiology and pathogenesis of amyloid A (AA) amyloidosis that may occur as an occasional complication of chronic inflammatory and infectious diseases are poorly understood. The preamyloid phase of experimentally induced AA amyloidosis can be greatly shortened in recipient animals by intravenous or intraperitoneal transfer of amyloid enhancing factor (AEF) when there is a concomitant inflammatory episode. AEF is an operational term applied to poorly characterized tissue extracts and increased AEF activity that precedes amyloid deposition. We now report that AA is rapidly formed in mice following oral administration of an AEF preparation that does not contain AA peptides. This finding indicates that a transmissible agent present in diet may be a contributory factor in amyloid fibril formation.
Elliott-Bryant
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Edith Nourse Rogers Memorial Veterans Administration Hospital, Bedford, Massachusetts, 01730, USA.
Cathcart
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D000284:Administration, Oral; D000686:Amyloidosis / Q000209:etiology* / Q000378:metabolism; D000818:Animals; D004032:Diet / Q000009:adverse effects; D004195:Disease Models, Animal; D005260:Female; D006023:Glycoproteins / Q000008:administration & dosage* / Q000302:isolation & purification; D051379:Mice; D008808:Mice, Inbred CBA; D000685:Serum Amyloid A Protein / Q000378:metabolism; D013154:Spleen / Q000378:metabolism / Q000473:pathology
D006023:Glycoproteins; D000685:Serum Amyloid A Protein; C046748:amyloid enhancing factor