The role of inflammatory cells in the pathogenesis of amyloidosis.
In the presence of amyloid enhancing factor, a variety of inflammatory stimuli, many of them nonantigenic, trigger amyloid deposition in 48 hours. There is a striking correlation between the extent of splenic amyloid deposition and the severity of inflammation at the injection site of the various irritants. Sublethal irradiation results in a parallel effect on the local inflammatory response and the accompanying extent of amyloid deposition produced in the spleen. Evidence that a product of local acute inflammatory responses is related to the deposition of amyloid is also presented. It is proposed that this product is a protease derived from the infiltrating polymorphonuclear leukocytes.
D000208:Acute Disease; D000686:Amyloidosis / Q000209:etiology* / Q000473:pathology; D000818:Animals; D001391:Azo Compounds; D002364:Caseins; D004195:Disease Models, Animal; D005122:Exudates and Transudates / Q000166:cytology; D005260:Female; D007249:Inflammation / Q000150:complications* / Q000473:pathology; D051379:Mice; D008808:Mice, Inbred CBA; D009504:Neutrophils / Q000502:physiology; D013158:Splenic Diseases / Q000209:etiology
D001391:Azo Compounds; D002364:Caseins