Secondary amyloidosis in normal and immunocompromised mice infected with Schistosoma japonicum.
Secondary amyloidosis developed in various tissues of immunologically intact and T-cell deprived CBA mice infected with Schistosoma japonicum as indicated by histological, histochemical and immunofluorescence techniques. Mice deprived of T-cells were most susceptible both in terms of the timing of the onset of amyloidosis, first noted 6 weeks post-infection, and in terms of the incidence, reaching 100% 12 weeks post-infection. Amyloidosis developed later in the infection in immunologically intact mice, the incidence was lower and there was less extensive replacement of normal tissue compared with that seen in T-cell deprived mice. Amyloid-related changes were most noticeable in the spleen where there was replacement of both follicular and non-follicular tissue. In the liver, amyloid deposits caused hepatocellular atrophic changes and in the kidney, glomerular and interstitial deposits were observed. The relationships between immunological reactivity and amyloidosis during schistosome infection is discussed.
D000686:Amyloidosis / Q000473:pathology*; D000818:Animals; D007153:Immunologic Deficiency Syndromes / Q000473:pathology*; D007668:Kidney / Q000473:pathology; D008099:Liver / Q000473:pathology; D008212:Lymphocyte Depletion; D051379:Mice; D008808:Mice, Inbred CBA; D012554:Schistosomiasis japonica / Q000473:pathology*; D013154:Spleen / Q000473:pathology / Q000648:ultrastructure; D013997:Time Factors