Acceleration of murine AA amyloid deposition by bovine amyloid fibrils and tissue homogenates

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Abstract
Acceleration of amyloid deposition by administration of amyloid fibrils and transmissibility of disease have been reported for several types of amyloidosis. Reactive amyloidosis (AA) occurs in a wide variety of domestic animal species and is characterized by amyloid deposition mainly in spleen, liver, and kidneys. Because the visceral organs of domestic animals have traditionally been used in Asian cuisines, it is important to examine whether dietary ingestion of the organs themselves (rather than purified amyloid fibrils) accelerates AA amyloid deposition. Herein, we show that murine AA amyloidosis develops rapidly after intraperitoneal or oral administration of purified amyloid fibrils or homogenates of amyloid-laden bovine liver. The amyloidosis development in mice was dependent on the concentration of amyloid fibrils or amyloidotic liver homogenates. We found that experimental murine AA amyloidosis was accelerated by dietary ingestion of both purified amyloid fibrils and tissue homogenates that contain amyloid fibrils. We also investigated livers of beef cattle and food chickens to examine whether they contain amyloid-enhancing factor activity. By microscopic examination of hematoxylin and eosin- and Congo red-stained sections, no amyloid deposition was detected in these livers, and no effective activity for experimental induction of AA amyloidosis in mice was detected in homogenates of these livers.

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