Regulation of Granulomatous Inflammation in Experimental Models of Schistosomiasis

Stavitsky, Abram B.

doi:10.1128/iai.72.1.1-12.2004

Cited by 63 publications

(57 citation statements)

References 144 publications

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“…The same observation had been made by Lewert and Mandlowitz(1969);Hang et al(1974); Montesano et al(1999);Stavitsky ( 2004) and Attallah et al (2006). The reduced size of granulomas observed by many authors and in our experiment in congenitally exposed kittens may be attributed to attenuated Th2 response.…”

Section: Discussionsupporting

confidence: 91%

Several Immunological Parameters in Rabbit Kittens Born to S. japonicum -infected Mothers

Abdel-Moneim¹,

Mutaz²

2014

GJBS

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In this study we explored the rabbit as an animal model for the congenital infection of schistosomiasis japonica and assessed the effect of a congenital S. japonicum infection on the resistance of rabbit kittens to a postnatal challenge infection. Kittens were challenged 17-19 weeks after the primary infection of their mothers. Perfusion was undertaken six weeks after the challenge. At this time parasitological, pathological and immunological parameters, worm reduction rate, granuloma size reduction rate, egg reduction rate, IgG and IgM responses were assessed and compared to that of kittens born to un-infected mothers. The overall prevalence of congenital infection in kittens of infected mothers was 20% (12/60). After a postnatal challenge infection, prenatally infected kittens had a 54.66% worm reduction rate, 41.45% egg reduction rate, and 51.76%granuloma size reduction rate compared to naive kittens. Congenital infection decreases the IgM responses by 39.47 % while it increases the IgG responses by 56.22 %. Together, these results indicate that congenital infection induce long-term effects on pathology and immune response patterns in rabbits subsequently challenge with S. japonicum cercariae.

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Section: Discussionsupporting

confidence: 91%

Several Immunological Parameters in Rabbit Kittens Born to S. japonicum -infected Mothers

Abdel-Moneim¹,

Mutaz²

2014

GJBS

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“…Obesity is also predictive of the presence of fibrosis, potentially progressing to advanced liver disease (Festi et al 2004). Schistosomiasis mansoni infection also promotes liver injury in both humans and mice yet a granulomatous inflammation is formed around mature egg (Hogan et al 2002, Stavitsky 2004). In the former, liver dysfunction, dyslipidemia, and protein alteration are common findings (Lima et al 1998).…”

mentioning

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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“…[1][2][3] Interleukins (ILs)-4, -5, -9, and -13 are upregulated in the local microenvironment surrounding parasite ova accompanied by an influx of eosinophils, goblet cell hyperplasia, and increased IgG1 and IgE production. 4 Studies using both experimental infection with S. mansoni larvae and synchronous egg-induced lung granulomas have demonstrated critical, yet independent, roles for IL-4 and IL-13.…”

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confidence: 99%

TH1-Dominant Granulomatous Pathology Does Not Inhibit Fibrosis or Cause Lethality during Murine Schistosomiasis

Leeto

Herbert

Marillier

et al. 2006

The American Journal of Pathology

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Regulation of Granulomatous Inflammation in Experimental Models of Schistosomiasis

Cited by 63 publications

References 144 publications

Several Immunological Parameters in Rabbit Kittens Born to S. japonicum -infected Mothers

Several Immunological Parameters in Rabbit Kittens Born to S. japonicum -infected Mothers

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

TH1-Dominant Granulomatous Pathology Does Not Inhibit Fibrosis or Cause Lethality during Murine Schistosomiasis

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