Pancreatic hepatocytes in hamsters ( Mesocricetus auratus) infected with Trypanosoma cruzi

Abstract

Hepatocytic metaplasia may be induced in hamsters by carcinogens, and associated with aging, diabetes or chronic pancreatitis. By means of histopathologic and immunohistochemic studies, we observed pancreatic hepatocytes in hamsters infected and reinfected with Trypanosoma cruzi. The change was seen in 18 (19%) out of 94 infected animals, and was not found among 53 controls, Normal islet cells were immunoreactive for neuron-specific enolase and not reactive for NCL-HAS. Metaplastic cells were immunoreactive for NCL-HAS and not reactive for islet hormones and enolase. No relationship was observed between number of inoculations and metaplasia; however, the intensity of the inflammatory process and sequels seems to favor the development of metaplastic cells. Hamsters infected with T. cruzi may be useful to study hepatocytic metaplasia, and contribute to clarify aspects of Chagas' disease and pancreatic changes. Our data indicate that aging, in addition to inflammation and atrophy, plays a role in this change. Index Descriptors and Abbreviations: Hamster; Experimental Chagas' disease; Chronic pancreatitis; Pancreatic hepatocytes; Hepatocytic metaplasia; BSA, bovine serum albumin; HE, hematoxylin and eosin; mtDNA, mitochondrial DNA; NCL-HAS, Novocastra-hepatocyte-specific antigen assay; PAP, peroxidase–antiperoxidase; PH, pancreatic hepatocytes; PI, pancreatic islets; PI/s, number of pancreatic islets per section.