Sequence and preliminary characterisation of a Taenia saginata oncosphere gene homologue of the small heat-shock protein family

During antibody screening of a Taenia saginata oncosphere cDNA library a clone (R-Tso2) sharing a high degree of homology at both the DNA and amino acid levels with the small heat-shock protein (shsp) family was identified. The R-Tso2 clone was a full-length sequence (1162 bp) with an open reading frame of 945 bp and 314 amino acids, corresponding to a deduced molecular mass of 35.6 kDa and isoelectric point of 5.6. R-Tso2 had the highest degree of homology with the Schistosoma mansoni major egg antigens, showing the characteristic shsp 100 amino-acid sequence motif duplicated. The R-Tso2 expression product was not immuno-precipitated by any serum from a panel of serum samples obtained from bovine, porcine and human hosts suffering from either T. saginata or T. solium cysticercosis. Received: 22 June 1997 / Accepted: 30 October 1997     

Schistosoma haematobium,S. intercalatum,S. japonicum,S. mansoni,and S. rodhaini in mice: relationship between patterns of lung migration by schistosomula and perfusion recovery of adult worms

The development of five schistosome species was compared in mice by the recovery of schistosomula from chopped lung tissue and of adult worms by portal perfusion. Three developmental patterns appeared. (1) Schistosoma japonicum was unique in showing an early establishment of schistosomula in and a rapid departure from the lungs together with the highest worm recovery; (2) S. haematobium contrasted by establishing later and persisting in the lungs for at least 2 weeks while yielding the lowest adult worm recovery; and (3) S. intercalatum, S. mansoni, and S. rodhaini had an intermediate pattern – they resided in the lungs for several days, then disappeared and produced intermediate numbers of adults. Lung petechiae, known to accompany the migration of S. japonicum, were never detected after infection with the other species. We speculate that the three migration patterns of schistosomes are related to the size of the relative spectra of naturally infected definitive hosts. Received: 31 August 1997 / Accepted: 15 October 1997     

Effects of benzimidazole anthelmintics as microtubule-active drugs on the synthesis and transport of surface glycoconjugates in Hymenolepis microstoma, Echinostoma caproni, and Schistosoma mansoni

Hymenolepis microstoma (Cestoda), Echinostoma caproni, and Schistosoma mansoni (Digenea) were exposed to benzimidazoles to determine the influence of the drugs on the secretion of glycoconjugates that protect the worms' surface. Worms were obtained from mice treated with mebendazole or albendazole, and the glycoconjugates were localized in the parasite tissues by cytochemistry using lectin-gold conjugates. Events leading to the death of H. microstoma and E. caproni extended over a medication period for at least 2–3 days, and the following interrelated phases were discernible. Upon depolymerization of the microtubules the tegumentary cytons continued to synthesize glycoconjugates for up to about 24 h. Vesicles containing the glycans accumulated in the cytons, but their microtubule-based transport to the distal tegument was inhibited. At about 1 day the Golgi complex became fragmented and the production of glycans sharply declined. As a consequence of this and an ongoing turnover of the surface coat the contents of glycoconjugates in the distal tegument decreased. Similar effects were produced by vinblastine and colchicine in vitro. In contrast, benzimidazole treatment of S. mansoni, which is reportedly inefficacious, did not alter the replenishment of the surface glycoconjugates. Diminution of the coating with glycoconjugates of the surface of drug-sensitive species constitutes a secondary effect of benzimidazoles that might, synergistically with immune mechanisms of the host, enhance the expulsion of the worms. Received: 18 October 1997 / Accepted: 10 November 1997     

Host range of poliovirus is restricted to simians because of a rapid sequence change of the poliovirus receptor gene during evolution

Summary.  The host range of most poliovirus (PV) strains is restricted to simians. This host range specificity is believed to be determined by the interaction between PV and its receptor molecule. To elucidate the molecular basis of this species-specific infection of PV, we cloned orthologs of the PV receptor (PVR) gene (pvr) as well as those of PV receptor-related genes 1 and 2 (prr1 and prr2) from various mammalian species. These three genes are widely present in mammalian genomes including those of non-susceptible species. Comparison of the deduced amino acid sequences of PVR orthologs revealed that the NH₂-terminal immunoglobulin-like domain (domain 1), which is the virus binding site in the human PVR, is highly variable among species, whereas that of PRR1 is highly conserved. Domain 1 of the PVR orthologs for the ring-tailed lemur and rabbit, which are not susceptible to PV, show only 51 and 61% amino acid sequence identity to that of human PVR, respectively. Chimeric PVR proteins that have the domain 1 of the ring-tailed lemur and rabbit PVRs failed to serve as receptors for PV. These results suggest that rapid changes in the domain 1 sequence during mammalian evolution determined the host range restriction of PV. Note: Nucleotide sequence data reported are available in the DDBJ/EMBL/ GenBank databases under the following accession numbers; brown capuchin pvr: AB086124 to AB086131, ring-tailed lemur pvr: AB086132 to AB086137, rabbit pvr: AB086138 to AB086144, pvr gene fragment of squirrel monkey: AB086252, gorilla: AB086253, common marmoset: AB086254, chimpanzee: AB086255, prr1 gene fragment of African green monkey: AB086001, bovine: AB086002, brown capuchin: AB086003, squirrel monkey: AB086004, ring-tailed lemur: AB086005, rabbit: AB086006, gorilla: AB086007, dog: AB086008, common marmoset: AB086009, dolphin: AB086010, chimpanzee: AB086145, and mole: AB086146. prr2 gene fragment of African green monkey: AB086147, bovine: AB086148, brown capuchin: AB086149, squirrel monkey: AB086150, ring-tailed lemur: AB086151, rabbit: AB086152, gorilla: AB086153, dog: AB086154, common marmoset: AB086155, dolphin: AB086156, chimpanzee: AB086157, mole: AB086158. Received June 14, 2002; accepted August 22, 2002     

Levels of Schistosoma mansoni Circulating Antigen in Chronic Hepatitis C Patients with Different Stages of Liver Fibrosis

The goal of this study was to determine the levels of S. mansoni antigen in different liver fibrosis stages with chronic hepatitis C (CHC) Egyptian patients. A total of 174 CHC patients showing HCV-NS4 antigen and HCV- RNA in their sera were included. S. mansoni antigen was detected in serum using Western blot and ELISA. The levels of interferon-γ (IFN- γ) were determined using ELISA. The 50 kDa S. mansoni antigen discriminated patients infected with S. mansoni from healthy individuals with 0.93 area under curve (AUC), 92% sensitivity, and 97% specificity. The level of S. mansoni antigen (μg/ml) was significantly (P < 0.0001) increased with the progression of liver fibrosis stages (26.9 ± 17.5 in F1, 42.1 ± 25.2 in F2, 49.8 ± 30.3 in F3 and 62.2 ± 26.3 μg/mL in F4 liver cirrhosis), 26.9 ± 17.59 in significant fibrosis (F2–F4); 51.2 ± 27.9 in advanced fibrosis (F3–F4). A significant correlation (r = 0.506; P < 0.0001) was shown between the levels of the S. mansoni antigen and the HCV-NS4 antigen. In conclusion, the presence of S. mansoni antigen in different liver fibrosis stages of CHC patients confirming that concomitant schistosome infection aggravates liver disease.     

Papain‐Based Vaccination Modulates Schistosoma mansoni Infection‐Induced Cytokine Signals

We have previously shown that immunization of outbred rodents with cysteine peptidases‐based vaccine elicited type 2‐biased immune responses associated with consistent and reproducible protection against challenge Schistosoma mansoni. We herein start to elucidate the molecular basis of C57BL/6 mouse resistance to S. mansoni following treatment with the cysteine peptidase, papain. We evaluated the early cytokine signals delivered by epidermal, dermal, and draining lymph node cells of naïve, and S. mansoni ‐infected mice treated 1 day earlier with 0 or 50 μg papain, or immunized twice with papain only (10 μg/mouse), papain‐free recombinant S. mansoni glyceraldehyde 3‐phosphate dehydrogenase and 2‐Cys peroxiredoxin peptide (10 and 15 μg/mouse, respectively = antigen Mix), or papain‐adjuvanted antigen Mix. Schistosoma mansoni infection induced epidermal and lymph node cells to release type 1, type 2 and type 17 cytokines, known to counteract each other. Expectedly, humoral immune responses were negligible until patency. Papain pretreatment or papain‐based vaccination diminished or shut off S. mansoni infection early induction of type 1, type 17 and type 2 cytokines except for thymic stromal lymphopoietin and programmed the immune system towards a polarized type 2 immune milieu, associated with highly significant (P < 0.005 – <0.0001) resistance to S. mansoni infection.     

Follow-up of four HIV-infected individuals after administration of hepatitis C virus and GBV-C/hepatitis G virus contaminated intravenous immunoglobulin: Evidence for HCV but not for GBV-C/HGV transmission

In 1994, hepatitis C virus (HCV) infection was transmitted to four HIV seropositive patients attending the Department of Angiology, University Clinics, Frankfurt am Main, by the administration of Gammagard®. The patients were suffering from thrombocytopenia and received betweeen 20 and 30 g of the contaminated lot 93F21AB11. GBV-C/HGV RNA could be amplified from the Gammagard® lot 93F21AB11 using 5′NCR and NS5 primer pairs. All the four patients were negative in the GBV-C/HGV RT-PCR prior to therapy and until the end of the follow-up period. GBV-C/HGV IgG antibodies to the putative envelope (E2) were detected using the E2 HGV-env kit (Boehringer-Mannheim, Germany) in Gammagard® lot 93F21AB11 and in one patient before donation of immunoglobulin. Anti-E2 seroconversion was observed in one recipient, the other two patients remained anti-E2 seronegative until the end of the observation period. It is concluded that there is no direct evidence for transmission of GBV-C/HGV by contaminated intravenous immunoglobulin since GBV-C/HGV RNA was not detected in the recipients up to 1 year after administration. J. Med. Virol. 53:25–30, 1997. © 1997 Wiley-Liss, Inc.     

Susceptibility of neonate mice born to Schistosoma mansoni-infected and noninfected mothers to subsequent S. mansoni infection

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.     

Heterogeneity of class I and class II MHC sequences in Schistosoma mansoni

We investigated the genetic variations in class I and class II major histocompatibility complex (MHC) genes of Schistosoma mansoni and the effects of host MHC genotypes. S. mansoni was maintained in combinations of two mouse strains with different MHC genotypes, and the MHC gene sequences of the cercariae were investigated. The detected class I MHC gene sequences were variable, with high similarity between the H-2D^b murine host and the parasite. For other combinations, however, the parasite sequence was homologous to those of anthropoids. All class II MHC sequences detected in S. mansoni were homologous to those of anthropoids. Our results suggest that the genetic variation in the MHC sequences of S. mansoni is derived in part from the current host, indicating horizontal transfer of the sequences from mammal to parasite.     

Antigenic cross‐reactivity between Schistosoma mansoni and peanut: a role for cross‐reactive carbohydrate determinants (CCDs) and implications for the hygiene hypothesis

The antigenic reactivity of constituents of Schistosoma mansoni and peanut (Arachis hypogaea) was investigated to determine whether identical antigenic epitopes possessed by both organisms provided a possible explanation for the negative correlation between chronic schistosome infection and atopy to allergens. Aqueous extracts of peanuts were probed in Western immunoblots with rabbit IgG antibodies raised against the egg, cercarial and adult worm stages of S. mansoni. Several molecules in the peanut extract were antigenically reactive with antibodies from the various rabbit anti‐schistosome sera. A pair of cross‐reactive peanut molecules at ~30 000–33 000 molecular weight was purified and both proteins were identified by mass spectrometric analysis as the peanut allergen Ara h 1. Anti‐S. mansoni soluble egg antigen antibodies that were eluted off the peanut molecules reacted with two S. mansoni egg antigens identified by mass spectrometry as IPSE/α‐1 and κ‐5. Alignments of the amino acid sequences of Ara h 1 and either IPSE/α‐1 or κ‐5 revealed a low level of peptide sequence identity. Incubation of nitrocellulose paper carrying electrophoresed peanut molecules, six constituents of other allergic plants and S. mansoni egg antigens in a mild solution of sodium metaperiodate before probing with antibodies, inhibited most of the cross‐reactivities. The results are consistent with the antigenic cross‐reactive epitopes of S. mansoni egg antigens, peanut and other allergic plants being cross‐reactive carbohydrate determinants (CCDs). These findings are novel and an explanation based on ‘blocking antibodies’ could provide an insight for the inverse relationship observed between schistosome infection and allergies.     

Experimental double infection of Biomphalaria glabrata snails with Angiostrongylus cantonensis and Schistosoma mansoni

Summary Two groups of Biomphalaria glabrata snails primarily infected with Angiostrongylus cantonensis were secondarily exposed to infection with Schistosoma mansoni. To investigate any antagonistic effect of a first infection on a superimposed one and to compare to singly and non-infected snails, a series of experiments was undertaken in which snails were individually exposed, variously, to 1,000 and 2,000 first-stage larvae of A. cantonensis and then to 5 and 10 miracidia of S. mansoni 1 day and 3 weeks later.Snails became infected with S. mansoni in both groups of snails with double infections and shed cercariae after the same incubation period as in the singly infected groups. The number of snails shedding cercariae simultaneously was similar in single and double infection groups during the first two weeks of shedding, after which this number decreased somewhat in doubly infected groups. Snails with double infection showed higher cumulative mortality rates than in snail groups with single infection with either A. cantonensis or S. mansoni. Therefore, initial infection of B. glabrata with A. cantonensis produced no inhibitory or retarding effect on subsequent infection of snails with S. mansoni.

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Zusammenfassung Zwei Gruppen der Süßwasserschnecke Biomphalaria glabrata, die zuvor mit 1000 bzw. 2000 ersten Larven von Angiostrongylus cantonensis pro Schnecke infiziert worden waren, wurden zur Feststellung eines eventuellen antagonistischen Effekts zwischen beiden Parasiten, einen Tag und drei Wochen später mit 5 bzw. 10 Miracidien von Schistosoma mansoni infiziert. Nicht infizierte und mit jeweils nur einer der beiden Parasitenarten infizierte Schnecken dienten als Kontrolle.In beiden doppelt infizierten Gruppen ging die S. mansoni-Infektion sehr gut an, und die Ausscheidung von Cercarien begann nach der gleichen Entwicklungszeit wie bei den nur mit S. mansoni infizierten Kontrollgruppen. Die Anzahl Cercarien ausscheidender Schnecken war in den beiden ersten Wochen bei den jeweils einzeln und doppelt infizierten Gruppen sehr ähnlich, während sie sich in der Folgezeit in den doppelt infizierten Gruppen rasch verminderte. In Gruppen mit Doppelinfektion zeigte sich eine höhere Mortalität als bei den jeweils nur mit A. cantonensis oder S. mansoni infizierten Schnecken. Eine Beeinflussung der Entwicklung von S. mansoni durch die vorausgegangene Nematodeninfektion konnte nicht nachgewiesen werden.

     

The S. mansoni glycoprotein ω-1 induces Foxp3 expression in NOD mouse CD4⁺ T cells

Immunization with Schistosoma mansoni soluble antigen preparations protects non‐obese diabetic (NOD) mice against the development of type 1 diabetes. These preparations have long been known to induce Th2 responses in vitro and in vivo. Recently, two separate groups have reported that ω‐1, a well‐characterized glycoprotein in S. mansoni soluble egg antigens (SEA), which with IL‐4 inducing principle of S. mansoni eggs (IPSE/α‐1) is one of the two major glycoproteins secreted by live eggs, is a major SEA component responsible for this effect. We found that ω‐1 induces Foxp3 as well as IL‐4 expression when injected in vivo. We confirmed that ω‐1 conditions DCs to drive Th2 responses and further demonstrated that ω‐1 induces Foxp3⁺ T cells from NOD mouse naïve T cells. In contrast, IPSE/α‐1 did not drive Foxp3 responses. The in vitro development of Foxp3‐expressing T cells by ω‐1 was TGF‐β‐ and retinoic acid‐dependent. Our work, therefore, identifies ω‐1 as an important factor for the induction of Foxp3⁺ T cells by SEA in NOD mice.     

A monoclonal antibody against Schistosoma haematobium soluble egg antigen: efficacy for diagnosis and monitoring of cure of S. haematobium infection

A monoclonal antibody (mAb), 2F/11F, raised against Schistosoma haematobium soluble egg antigen (SEA) was found to be nonreactive with S. mansoni SEA or other parasite antigens (Fasciola hepatica, Echinococcus granulosus). This IgG₁ mAb recognized a repetitive epitope on S. haematobium SEA in the molecular-weight regions of 70, 42, and 35 kDa. It was employed as both an antigen-capture and a biotinylated detection antibody in a sandwich enzyme-linked immunosorbent assay (ELISA) for the detection of circulating schistosome antigen (CSA) and had a detection limit of <1 ng S. haematobium SEA/ml. CSA levels were measured in serum and urine samples from 116 S. haematobium-infected rural students before therapy and at 4, 8, and 12 weeks after praziquantel treatment. Serum and urine samples from 50 S. mansoni -infected patients, 15 patients harboring other parasites, and 30 noninfected individuals were also assessed. CSA was detected in 90.5% of serum samples and 94% of urine samples from S. haematobium-infected patients. CSA was undetectable in serum from the 15 patients harboring other parasites and in 94% of serum samples and 84% of urine samples from S. mansoni-infected patients. In the S. haematobium-infected group a positive correlation was detected between CSA levels in serum and urine samples and the egg load per 10 ml urine. A significant reduction in CSA levels was detected in serum and urine samples after praziquantel therapy. CSA was undetectable in 87% of serum samples and 81.5% of urine samples from schistosomiasis haematobium patients at 12 weeks post-treatment. These data demonstrate that the use of mAb 2F/11F for detection of CSA provides a sensitive method for the immunodiagnosis and monitoring of cure of schistosomiasis haematobium. Received: 5 December 1998 / Accepted: 26 June 1999     

Serum levels of circulating anodic antigen and circulating cathodic antigen detected in mice infected withSchistosoma japonicum orS. mansoni

Serum concentrations of circulating anodic antigen (CAA) and circulating cathodic antigen (CCA) were studied in mice infected with eitherSchistosoma japonicum orS. mansoni cercariae. Sera from uninfected mice were negative for both antigens. CAA was detectable in theS. japonicum-infected mice as early as at 2 weeks post-infection (p.i.), and levels were higher in these animals than in theS. mansoni-infected group during the full study period. At the moment of perfusion, 10 weeks p.i., a median of 9 and 29 worms, respectively, were recovered from theS. japonicum-andS. mansoni-infected mice, and the median CAA levels were 326 and 27 ng/ml, respectively. In contrast, CCA levels were much lower in theS. japonicum-infected group (27 ng/ml) as compared with theS. mansoni-infected mice (282 ng/ml). These results suggest an important difference betweenS. japonicum andS. mansoni infections in CAA and CCA production and/or clearance and indicate a significant role for CAA in the diagnosis of human schistosomiasis japonicum.     

Ellagic acid reduces murine schistosomiasis mansoni immunopathology via up-regulation of IL-10 and down-modulation of pro-inflammatory cytokines production

Context: The main immunopathology in schistosomiasis mansoni consists of a granulomatous inflammatory and fibrosing reaction in the liver and intestine against tissue trapped parasite eggs, which is mediated by CD4^+?T cells. Ellagic acid (EA), a natural phenolic compound found in fruits and nuts, has potent anti-oxidant and anti-inflammatory properties.

Objective: The aim of the present study was to evaluate the potential effect of EA in the treatment of murine schistosomiasis mansoni and its induced immunopathology.

Materials and methods: Mice were infected, each with 40 Schistosoma mansoni (S. mansoni) cercariae and treated with EA at a total dose of 600?mg/kg body weight. At week eight of infection, mice were sacrificed; worm and egg burden were estimated; hepatic granuloma volume and collagen fibers deposition were evaluated; splenocytes were prepared and cultured in the presence of S. mansoni antigens.

Results: EA treatment did not show any significant effect on worm or egg burden. However, hepatic granuloma volume and collagen fibers deposition were largely reduced with EA treatment. EA treatment augmented specific IL-10 production in response to S. mansoni antigenic stimulation. However, specific IL-1β, IL-4, IL-12, IL-13, IL-17A, TNF-α and IFN-γ production were significantly reduced with ex vivo and in vivo EA treatment. Serum IgM and IgG levels significantly increased, whereas specific IgA and IgE levels did not significantly change with EA treatment.

Conclusion: EA treatment modulates cellular and humoral immune responses of infected mice and leads to a significant reduction of liver pathology in acute murine schistosomiasis mansoni.     

Type I interferons provide additive signals for murine regulatory B cell induction by Schistosoma mansoni eggs

The helminth Schistosoma mansoni (S. mansoni) induces a network of regulatory immune cells, including interleukin (IL)‐10‐producing regulatory B cells (Bregs). However, the signals required for the development and activation of Bregs are not well characterized. Recent reports suggest that helminths induce type I interferons (IFN‐I), and that IFN‐I drive the development of Bregs in humans. We therefore assessed the role of IFN‐I in the induction of Bregs by S. mansoni. Mice chronically infected with S. mansoni or i.v. injected with S. mansoni soluble egg antigen (SEA) developed a systemic IFN‐I signature. Recombinant IFN‐α enhanced IL‐10 production by Bregs stimulated with S. mansoni SEA in vitro, while not activating Bregs by itself. IFN‐I signaling also supported ex vivo IL‐10 production by SEA‐primed Bregs but was dispensable for activation of S. mansoni egg‐induced Bregs in vivo. These data indicate that although IFN‐I can serve as a coactivator for Breg IL‐10 production, they are unlikely to participate in the development of Bregs in response to S. mansoni eggs.     

Heterologous immunity againstSchistosoma mansoni in mice by administration ofHeterobilharzia americana

Three groups of Swiss albino mice were exposed to cercariae ofHeterobilharzia americana a mammalian schistosome in Southern United States. They were challenged at different intervals with cercariae of a Puerto Rican strain ofSchistosoma mansoni, and a fourth group (control for the first two groups) was exposed only toS. mansoni. With a patent infection (two months) ofH. americana there was a noticeable reduction of the worm recovery rates ofS. mansoni and its eggs deposited in the tissues. In the two other groups exposed simultaneously or at a 3-week interval, there was no significant reduction in the recovery rates of adultS. mansoni and the number of eggs exceeded in some cases that noted for the control group. Thus a patent infection withH. americana is necessary to confer immunity against a challenge infection withS. mansoni.     

Parthenogenesis in the genusSchistosoma: Electrophoretic evidence for this reproduction system inS. japonicum andS. mansoni

Mixed infections withSchistosoma japonicum andS. mansoni were carried out in mice.S. japonicum females paired withS. mansoni males developed normally and produced numerous viable eggs; very little sperm was found in the female genital tract. The eggs yielded many miracidia infective toOncomelania hupensis, the host ofS. japonicum. Cercariae arising from miracidia developed into male worms with an electrophoretic pattern of malate dehydrogenase (MDH) corresponding only to mae maternal speciesS. japonicum. S. mansoni females paired withS. japonicum produced few viable eggs; sperm was found in the female genital tract. Miracidia hatched from mime of these eggs were infective toBiomphalaria glabrata, the host ofS. mansoni. Cercariae arising from miracidia developed into female worms with an electrophoretic pattern of MDH typical of the maternal speciesS. mansoni. It was concluded thatS. japonicum females paired withS. mansoni males andS. mansoni females paired withS. japonicum males reproduce parthenogenetically. Parthenogenesis in schistosomes is discussed.     

Ultrastructural changes of kidney in Schistosoma mansoni-infected mice

Schistosomiasis is the second threatening parasitic disease after malaria and among Schistosoma spp., Schistosoma mansoni (S. mansoni) affects about 100 million people in tropic regions in Africa and South America. The current study was carried out to investigate ultrastructural changes of the kidney in mice infected with cercariae of S. mansoni, in which 20 Swiss albino mice of 60-day-old were assigned into two groups (10 each). Control group received 1 ml normal saline by intraperitoneal route. Model group were intraperitoneally infected with 1 ml normal saline containing 40 cercariae of S. mansoni/mouse. After 60 days of infection, specimens from the kidneys of both control and infected mice were obtained and processed for transmission electron microscopy (TEM) examination. The main ultrastructural changes were observed in both glomeruli and tubules. Glomerular findings included irregular thickening and splitting of the glomerular basement membrane (GBM), flattening and effacement of the foot processes of podocytes, and proliferation of mesangial cells. Tubular changes were in the form of swelling, atrophy and vacuolation of tubular epithelial cells, and presence of autophagic vacuoles. In conclusion, adopting TEM shows a number of ultrastructural changes in the kidneys of mice infected with cercariae of S. mansoni, most notably thickening and splitting of GBM and flattening and effacement of foot processes of podocytes and tubular autophagic vacuoles. These changes are still unraveled well in the literature.