Elliott-Bryant R, Cathcart E S
Edith Nourse Rogers Memorial Veterans Administration Hospital, Bedford, Massachusetts, 01730, USA.
Clin Immunol Immunopathol. 1998 Jul;88(1):65-9. doi: 10.1006/clin.1998.4555.
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.
作为慢性炎症和感染性疾病的偶发并发症可能出现的淀粉样蛋白A(AA)淀粉样变性的病因和发病机制尚不清楚。当存在伴随的炎症发作时,通过静脉内或腹膜内转移淀粉样增强因子(AEF),实验性诱导的AA淀粉样变性的淀粉样前体阶段在受体动物中可大大缩短。AEF是一个应用于特征不明的组织提取物和淀粉样沉积之前AEF活性增加的操作性术语。我们现在报告,在口服不含AA肽的AEF制剂后,小鼠体内迅速形成AA。这一发现表明,饮食中存在的一种可传播因子可能是淀粉样纤维形成的一个促成因素。