Experimental models of Schistosoma mansoni infection

Cheever, Allen W.; Lenzi, J. A.; Lenzi, Henrique Leonel; Andrade, Zilton A.

doi:10.1590/s0074-02762002000700002

Cited by 120 publications

(106 citation statements)

References 259 publications

(215 reference statements)

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“…Therefore, schistosomiasis mansoni infection could overload hepatic injury on the basis of an already pathological situation. Eggs trapped in the liver lead to inflammation (Fallon & Dunne 1999, Cheever et al 2002, collagen deposition and fibrous expansion of the portal spaces and intrahepatic portal-vein obstruction (Abath et al 2006). The literature about liver histological changes in schistosomiasis mansoni is relatively abundant (Andrade et al 1997, Lenzi et al 1998, 1999, Baptista & Andrade 2005).…”

Section: Discussionmentioning

confidence: 99%

Hepatic stereology of schistosomiasis mansoni infected-mice fed a high-fat diet

Neves

Alencar

Águila

et al. 2006

Mem. Inst. Oswaldo Cruz

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High-fat diets induce weight gain and fatty liver in wild-type mice. Schistosomiasis mansoni infection also promotes hepatic injury. This study was designed to quantify hepatic alterations in schistosomiasis mansoni infected mice fed a high-fat diet (IHFC) or standard chow (ISC), uninfected mice fed a high-fat diet (HFC) or standard chow (SC). Mice were sacrificed during early infection (9 weeks from exposure). The following hepatic biometry and the stereology parameters were determined: volume density (hepatocytes [h], sinusoids [s], steatosis [st] and hepatic fibrosis [hf]); numerical density (hepatocyte nuclei -Nv[h]); absolute number of total hepatocyte N[h], normal hepatocyte N[nh], and binucleated hepatocyte N[bh], percentage of normal hepatocyte P[nh] and binucleated hepatocyte P[bh]. IHFC and HFC groups exhibited TC, HDL-C, LDL-C, and body mass significantly greater (p < 0.05) than control group. No significant differences were found regards liver volume (p = 0.07). Significant differences were observed regards P[nh] (p = 0.0045), P[bh] (p = 0.0045), Nv[h] (p = 0.0006), N[h] (p = 0.0125), N[bh] (p = 0.0164) and N[nh] (p = 0.0078). IHFC mice group presented 29% of binucleated hepatocytes compared to HFC group (19%), ISC group (17%) and SC (6%

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Section: Discussionmentioning

confidence: 99%

Hepatic stereology of schistosomiasis mansoni infected-mice fed a high-fat diet

Neves

Alencar

Águila

et al. 2006

Mem. Inst. Oswaldo Cruz

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“…Thus, mouse experimental crosses have been a suitable strategy for mapping genes involved in different complex diseases including the immune response against S. mansoni (Rutitzky et al 2005;Smith et al 2009). Several studies report differences in the hepatic fibrosis or granuloma size in different inbreed mouse lines *Corresponding author: luispmoro@usal.es Luis Pérez del Villar et al 530 (Cheever 1986;Cheever et al 1983;Cheever et al 2002). C57/BL6 mice show the highest degree of resistance to schistosomiasis, whereas CBA/2J mice develop the severe form of murine schistosomiasis (Fanning et al 1981;Bosshardt et al 1997).…”

Section: Introductionmentioning

confidence: 99%

Identifying phenotypes involved in susceptibility to Schistosoma mansoni infection in F1B6CBA mice

Villar

Vicente

Blanco-Gómez

et al. 2014

Acta Parasitologica

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Schistosomiasis is a disease with a strong genetic component influenced by socioeconomic and ecological factors. Epidemiological studies have identified several genetic regions involved in the schistosomiasis susceptibility. However, it is not well known what physiological traits are predisposing to the disease. The study of experimental infections in inbred mouse strains with variable genetic susceptibility to the disease offers a good opportunity to tackle this question. F1B6CBA hybrid between the most divergent strains was infected in order to characterize the immunophenotypes that correlate with the susceptibility of schistosomiasis disease in mice. Complete blood counts and immunophenotype were determined at 0, 3, 6, and 9 weeks post infection. Nine weeks after cercariae exposure, animals were perfused and worm recovery was assessed. A large number of hepatic lesions, a reduction in the eosinophil and basophil count in the acute phase of infection and the decreased number of monocytes, neutrophils and B-lymphocytes are phenotypes associated with increased susceptibility to S. mansoni infection.

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“…Concerning Symmers' fibrosis (clay pipestem fibrosis), different experimental hosts have been tried (Cheever et al 2003), such as monkeys (Lichtemberg & Sadun 1968, Sadun et al 1970, Lichtemberg et al 1971, Damian et al 1976, Farah et al 2000, rabbits , pigs (Hurst et al 2000), and mice (Warren & DeWitt 1958, Andrade & Warren 1964, Cheever 1965, Warren 1968, Andrade 1987a, Andrade & Cheever 1993. In this last animal model, during mild (one to two pairs of worms) and prolonged (16 weeks or more) infections with Schistosoma mansoni, a picture mimicking "clay pipestem" fibrosis seen in humans with advanced schistosomiasis has been reproduced in outbred and in some strains of well-nourished inbred mice (Andrade & Cheever 1993), but not in undernourished outbred specimens (Coutinho et al 1997).…”

mentioning

confidence: 99%

Malnutrition and hepatic fibrosis in murine schistosomiasis

Coutinho

2004

Mem. Inst. Oswaldo Cruz

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Experimental models of Schistosoma mansoni infection

Cited by 120 publications

References 259 publications

Hepatic stereology of schistosomiasis mansoni infected-mice fed a high-fat diet

Hepatic stereology of schistosomiasis mansoni infected-mice fed a high-fat diet

Identifying phenotypes involved in susceptibility to Schistosoma mansoni infection in F1B6CBA mice

Malnutrition and hepatic fibrosis in murine schistosomiasis

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