Avaliação quantitativa e qualitativa das alterações no tecido esplênico de camundongos esquistossomóticos e dislipidêmicos

Abstract

The effect of the changes promoted by hypercholesterolemia and experimental schistosomiasis infection on splenic architeture has remained elusive. In this study, we investigated the qualitative and quantitative organization of the splenic tissue in the acute phase (ninth week) of Schistosoma mansoni infection of mice fed either a hypercholesterolemic (29% lipids) or a standard chow (12% lipids). Spleen volume was measured by Scherlis Method. Histological sections (5μm) were stained with hematoxylin-eosin, Lennert's Giemsa and Picrosirius. The splenic disorganization was evaluated by histopathology, morphometry and stereology. Our major findings demonstrated that both diet and infection determined perturbations in splenic compartments. Infected mice, regardless of diet, had larger spleen (Student s t-test, P=0.004) and disorganized splenic architecture than in corresponding uninfected mice, for which no histopathology was evident. The white pulp compartment was reduced, whereas red pulp and germinal center were enhanced (Student s t-test, P<0.01), as demonstrated by stereology. High-fat fed infected mice showed larger white pulp diameter (Student s t-test, P=0.013) than in corresponding uninfected mice. Microscopic examination of spleen from uninfected mice fed hypercholesterolemic chow showed that white pulp was reduced and indistinct. In addition, infected mice showed cellular infiltrates characterized by polymorfonuclear cells, with intensive lymphocytic mitosis and Mott cells. Hemosiderin deposits tended to be in less extent in infected mice compared with uninfected controls. The red pulp compartment showed a significantly (Student s t-test, P=0.008) increased average number of megakaryocytes compared with uninfected mice. Standard fed mice showed exudative-productive granuloma around schistosome eggs distributed only sparsely in the red pulp, whereas a tissue reaction characterized by a cell infiltration in high-fat fed mice was found. The results of the present study suggest that both fat diet intake and infection contributed to splenic disorganization