Abstract
Severe hepatosplenic injury of mansonian schistosomiasis is caused by Th2 mediated granulomatous response against parasite eggs entrapped within the periportal tissue. Subsequent fibrotic scarring and deformation/sclerosing of intrahepatic portal veins lead to portal hypertension, ascites, and oesophageal varices. The murine model of Schistosoma mansoni (S. mansoni) infection is suitable to establish the severe hepatosplenic injury of disease within a reasonable time scale for the development of novel antifibrotic or anti-infective strategies against S. mansoni infection. The drawback of the murine model is that the material prepared for complex analysis of egg burden, granuloma size, hepatic inflammation, and fibrosis is limited due to small amounts of liver tissue and blood samples. The objective of our study was the implementation of a macroscopic scoring system for mice livers to determine infection-related organ alterations of S. mansoni infection. In addition, an in vitro biosensor system based on the detection of hepatocellular injury in HepG2/C3A cells following incubation with serum of moderately (50 S. mansoni cercariae) and heavily (100 S. mansoni cercariae) infected mice affirmed the value of our scoring system. Therefore, our score represents a valuable tool in experimental schistosomiasis to assess severity of hepatosplenic schistosomiasis and reduce animal numbers by saving precious tissue samples.
Highlights
In the host adult Schistosoma mansoni (S. mansoni) worms are found within the mesenteric blood vessels around the sigmoid colon and the rectum, where the oviposition takes places [1]
S. mansoni infection resulted in significant increase of liver and spleen weights compared to healthy control mice (Figure 2(a))
The different infection intensities were reflected by marked differences in the macroscopic appearance of infected mice livers in mice infected with 100 S. mansoni cercariae (Figure 2(b))
Summary
In the host adult Schistosoma mansoni (S. mansoni) worms are found within the mesenteric blood vessels around the sigmoid colon and the rectum, where the oviposition takes places [1]. Schistosomal eggs induce a strong antibody response against soluble egg antigens that corresponds to a type 4 hypersensitivity reaction mediated by T-helper 2 (Th2) cells and alternatively activated macrophages. Th2 response directs periocular inflammation towards fibrous scarring with subsequent deformation and sclerosing of the intrahepatic portal veins whereby the arterial and ductular structures remain largely unaffected [3]. Due to high infection rates or repeated infections periportal (Symmers’ pipestem) fibrosis [4] occurs as mild chronic granulomatous hepatitis or advanced hepatosplenic manifestations with massive fibrosis, splenomegaly, portal hypertension, ascites, and esophageal varices
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