The present study tested the hypothesis that prenatal exposure of neonate Outbred albino mice to Schistosoma mansoni antigens (Ags) or antibodies (Abs) modulates their immunity against postnatal responses to infection. Persistence of maternal S. mansoni Abs and/or Ags in mice born to S. mansoni-infected mothers (IF-IMs) and noninfected mothers (IF-NMs) for up to 8 weeks after delivery was investigated. A higher level of anti-S. mansoni IgG Ab was detected in sera of 1-week-old mice born to IF-IM compared to controls. Then, immunoglobulin (Ig)G gradually decreased to the eight week. No anti-S. mansoni IgM Ab was detected in sera of these offspring at any week after delivery. Schistosoma Ags were detected in liver and kidney tissues of mice born to infected mothers. However, Ags decreased markedly till the sixth week in the liver but increased significantly at the sixth week in the kidney. Eight-week-old mice born to infected and noninfected mothers were infected with 200 S. mansoni ceracriae. Their sera and livers were collected for testing IgG and granuloma formation 6 weeks postinfection. Worms were collected via portal perfusion and counted. Anti-S. mansoni IgG level, size and number of liver granuloma, and worm burden were significantly reduced in the offspring of infected mothers. These data suggest that in utero exposure of Outbred albino mice to S. mansoni may attenuate the pathogenesis of S. mansoni in subsequent challenge.

Abstract. A 63-kD Schistosoma mansoni antigen was detected in 149 (86%) of 174 umbilical cord blood sera from infected women at delivery. Specific IgG antibodies to this antigen were also detected in 80% of cord blood sera. The 63-kD antigen showed the same molecular mass by Western blotting when isolated from cord blood, maternal blood, breast milk, and urine from women infected with S. mansoni. This antigen was detected in the urine of 25 infants born to infected mothers and followed for 18-24 months after delivery. It was also detected in some infants up to 21 days after parturition and then disappeared at 28 days, demonstrating the influence of breast-feeding on persistence of antigen in infants born to infected women. Thus, exposure to Schistosoma antigens and maternal antibodies to this organism may influence the developing immune responses to natural infection or vaccination of children born in endemic areas.

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The pathogenesis of Schistosoma mansoni infection is largely determined by host T-cell mediated immuneSchistosomiasis is a debilitating parasitic disease affecting about 200 million people in 70 countries in the world and is caused by one of the three different species of Schistosoma: S. mansoni, S. haematobium, and S. japonicum. The major pathology of these parasitic infections is associated with a host delayed type hypersensitivity reaction to parasitic egg and egg products. Granulomatous inflammation is a cellular hypersensitivity reaction mediated by egg antigen-specific, MHC class II-restricted, TCR αβ expressing, CD4 + T helper cells (Iacomini et al. 1995). Patients infected with S. mansoni mount cellular and humoral immune responses to soluble egg antigens derived from crude homogenates of eggs. Thus, the end result of host responses to schistosome eggs in the liver is advanced portal fibrosis with dense deposits of collagens in greatly expanded portal tracts (El-Zayadi 2004). The immune reaction produced by the body against the schistosomal infection is a double-weaponed arm. Unfortunately, the harmful weapon is the longest and the most powerful. That is the immune reaction against the schistosomal egg causing the schistosomal granuloma. The other weapon of the immune system that should be lengthened and empowered is the protective immune response against infection, egg production and/or the granuloma formation. Many researchers have been doing their best to get the suitable agent that can stimulate the maximal, specific immune response against schistosomiasis (Goes & Hirsch 1996).Considerable efforts have been exerted to determine which S. mansoni antigens induce and elicit T cell-mediated responses and granuloma formation (Goes & Hirsch 1996). Several laboratories have isolated various antigens from crude soluble egg anigens (SEA) and soluble worm antigens (SWAP), and investigated their role in serology, blastogenic reactions, and granuloma responses to SEA (Bahia-Oliveira et al. 1997). These studies revealed a variety of biologically active antigenic moeities derived from S. mansoni antigen preparations (Goes & Hirsch 1996). One antigen, Smp40 (major egg antigen p40), has been described as highly immunogenic in humans and has been cloned and sequenced (Cao et al. 1993). The Smp40 peptide has 354 amino acid residues and shares homologies with the family of heat shock proteins and α-crystallins. There is evidence that α-crystallins act as chaperone for other important egg antigens released during the migra- tion phase of the eggs in the hepatic system (Nene et al. 1986). The immune response to Smp40 and Smp40 overlapping peptides can be studied in the cellular proliferation assays with the addition of either anti-interleukin (IL)-10 or IL-2 to overcome anergy. In the last decade, substantial resources have been invested to identify, characterize, and purify various schistosome antigens for the purpose of designing and testing potential vaccines. In fact, elucidation of egg antigens has received much les...

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The current study is aimed at evaluating serum collagens and other serum biochemical markers as useful, non-invasive markers of hepatic fibrosis associated with chronic hepatitis C virus (HCV). Collagen types I, II, III, and IV were detected in serum using ELISA and Western blot techniques. The ELISA levels of collagen I, II, III, and IV increased significantly with the progression of fibrosis staging. Based on receiver-operating characteristic (ROC) curve analysis, the collagen type III (70 kDa) and type IV (200 kDa) were more useful than other serum bio-markers for differentiating severe fibrosis from mild fibrosis. Multivariate discriminant analysis (MDA) selected a fibrosis discriminant score (FDS) = [2.345 + Collagen III (microg/mL) x 1.923 + Collagen IV (microg/mL) x 1.544 + ALT (U/mL) x 0.005] - [albumin(g/L) x 0.046]. The FDS correctly classified 87% of the severe fibrosis patients at a cut-off score = 2.2 (i.e., more than 2.2 indicated severe fibrotic liver and less than 2.2 indicated mild fibrotic liver) with specificity of 97%. In a validation study, the FDS was applied to the second cohort of patients and the results were reproduced without significant difference. In conclusion, the developed four-parameter based FDS is useful for identifying severe liver fibrosis in patients with chronic HCV infection.

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