Calomys callosus: an alternative model to study fibrosis in Schistosomiasis mansoni: the pathology of the acute phase

Abstract

Twenty Calomys callosus, Rengger, 1830 (Rodentia-Cricetidae) were studied in the early stage of the acute schistosomal mansoni infection (42nd day). The same number of Swiss Webster mice were used as a comparative standard. Liver and intestinal sections, fixed in formalin-Millonig and embedded in paraffin, were stained with hematoxilin and eosin, PAS-Alcian Blue, pH = 1.0 and 2.5, Lennert's Giemsa, Picrosirius plus polarization microscopy, Periodic acid methanamine silver, Gomori's silver reticulin and resorcin-fuchsin. Immunohistological study (indirect immunofluorescence and peroxidase labeled extravidin-biotin methods) was done with antibodies specific to pro-collagen III, fibronectin, elastin, condroitin-sulfate, tenascin, alpha smooth muscle actin, vimentin and desmin. The hepatic granulomas were small, reaching only 27% of the volume of the hepatic Swiss Webster granuloma. They were composed mainly by large immature macrophages, often filled by schistosomal pigment, characterizing an exsudative-macrophage granuloma type. The granulomas were situated in the parenchyma and in the portal space. They were often intravascular, poor of extracellular matrix components, except fibronectin and presented, sometimes alpha smooth muscle actin and vimentin positive cells. The C. callosus intestinal granulomas were similar to Swiss Webster, showing predominance of macrophages. Therefore, the C. callosus acquire very well the Schistosoma mansoni infection, without developing strong hepatic acute granulomatous reaction, suggesting lack of histopathological signs of hypersensitivity.

Histoarchitecture of schistosomal granuloma development and involution: morphogenetic and biomechanical approaches

“…The anatomical scaffold of extracellular matrix of the involved tissue is generally completely destroyed, but scarce residual fibers remain, which are mainly of vascular origin. The murine peri-ovular reaction may occur inside or outside the vessels, as was also observed in human cases (Raso & Bogliolo 1970), and in the Calomys callosus model (Lenzi JA et al 1995). As infection goes on, little by little, a random reticular scaffold or mesh (see Table, Fig.…”

Natural Schistosoma mansoni infection in Nectomys squamipes: histopathological and morphometric analysis in comparison to experimentally infected N. squamipes and C3H/He mice

“…38) with variable number of eosinophils, surrounded or not by mononuclear cells or were small and constituted by a macrophagic central layer surrounded by a thin collagenous and reticular pseudocapsule (Figs 3,33,37,38). The frequent presence of intravascular granulomas as was seen in C. callosus (Lenzi et al 1995) may be due to a periovular reaction inside the vessels with less granulocytes than in mice, poor in proteolytic enzymes responsible for corrosion of the vascular walls.…”

“…squamipes like C. callosus (Lenzi et al 1995), presented peculiar granulomas consisting predominantly of large macrophages, many of them full of schistosome pigment, characterizing a exudative-macrophage granuloma type, usually smaller than the equivalent granuloma type in mouse. They were composed by large macrophages Hepatic schistosomal granulomas in experimentally infected Nectomys squamipes -Portal exudative-productive granulomas rich in eosinophils (Fig.…”

“…For instance, hepatic granulomas of Calomys callosus (Rodentia: Cricetidae) are 27% smaller than granulomas from albino mice at the same time of infection (Lenzi et al 1995). The granuloma variability is due to the fact that this organized structure is composed by host and parasite components, functioning as a hybrid interface between two different phylogenetic beings, depending, therefore, on the host epigenetic characteristics (Lenzi et al 1998a).…”

Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus infected with Trypanosoma cruzi

“…Adapted to laboratory studies (Mello 1982) this animal represents a very peculiar experimental model, with the capacity of to control the infection with virulent strains of T. cruzi as the Y strain (Mello 1979, Borges et al 1982. Interestingly, tissue lesions are precocious with intense inflammatory infiltrates and early fibrogenesis, with a spontaneous regression of inflammation and fibrosis (Andrade et al 1994, Lenzi et al 1995, Magalhães-Santos et al 2002, 2004.…”