Schistosomiasis

Tucker, Matthew S.; Karunaratne, Laksiri B.; Lewis, Fred A.; Freitas, Tori C.; Liang, Yung-san

doi:10.1002/0471142735.im1901s103

Cited by 129 publications

(145 citation statements)

References 56 publications

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“…parasites or 'unexposed'. The success rate of exposure (defined as the percentage of snails that go on to develop patent infections) is 80-100% for B. glabrata exposed to S. mansoni (Lewis et al, 1986) and 30-70% for B. truncatus exposed to S. haematobium (Tucker et al, 2013). Not all exposed snails in the group develop full, patent infections, but we assumed that exposed snails were infected for some to all of the experimental period.…”

Section: Animals and Aquariamentioning

confidence: 99%

Infection with schistosome parasites in snails leads to increased predation by prawns: implications for human schistosomiasis control

Swartz

Leo

Wood

et al. 2015

Journal of Experimental Biology

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Schistosomiasis -a parasitic disease that affects over 200 million people across the globe -is primarily transmitted between human definitive hosts and snail intermediate hosts. To reduce schistosomiasis transmission, some have advocated disrupting the schistosome life cycle through biological control of snails, achieved by boosting the abundance of snails' natural predators. But little is known about the effect of parasitic infection on predator-prey interactions, especially in the case of schistosomiasis. Here, we present the results of laboratory experiments performed on Bulinus truncatus and Biomphalaria glabrata snails to investigate: (i) rates of predation on schistosome-infected versus uninfected snails by a sympatric native river prawn, Macrobrachium vollenhovenii, and (ii) differences in snail behavior (including movement, refuge-seeking and anti-predator behavior) between infected and uninfected snails. In predation trials, prawns showed a preference for consuming snails infected with schistosome larvae. In behavioral trials, infected snails moved less quickly and less often than uninfected snails, and were less likely to avoid predation by exiting the water or hiding under substrate. Although the mechanism by which the parasite alters snail behavior remains unknown, these results provide insight into the effects of parasitic infection on predator-prey dynamics and suggest that boosting natural rates of predation on snails may be a useful strategy for reducing transmission in schistosomiasis hotspots.

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Section: Animals and Aquariamentioning

confidence: 99%

Infection with schistosome parasites in snails leads to increased predation by prawns: implications for human schistosomiasis control

Swartz

Leo

Wood

et al. 2015

Journal of Experimental Biology

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“…Cercariae, schistosomula, adult worms, and eggs were isolated and processed for parasite life-stage lysates or soluble egg antigen (SEA) as previously described (34,48). For SDS-PAGE and Western blotting, 1 g of SEA and 5 g parasite lysates were boiled in 1ϫ NuPAGE SDS sample buffer plus 2.5% ␤-mercaptoethanol for 10 min and then run in 10-well Mini-Protean-TGX gels at 200 V for 30 min with broad-range protein standards (Spectra multicolor).…”

Section: Methodsmentioning

confidence: 99%

“…Schistosomula were isolated as described previously (34,48). After vortex transformation, separation from tails via Percoll, and washing in DMEM, the newly transformed schistosomula were cultured for 3 h at 37°C in 96-well plates with 50 to 100 parasites in 40 l of DMEM with penicillin-streptomycin in each well.…”

Section: Methodsmentioning

confidence: 99%

Identification of Antigenic Glycans from Schistosoma mansoni by Using a Shotgun Egg Glycan Microarray

et al. 2016

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f Infection of mammals by the parasitic helminth Schistosoma mansoni induces antibodies to glycan antigens in worms and eggs, but the differential nature of the immune response among infected mammals is poorly understood. To better define these responses, we used a shotgun glycomics approach in which N-glycans from schistosome egg glycoproteins were prepared, derivatized, separated, and used to generate an egg shotgun glycan microarray. This array was interrogated with sera from infected mice, rhesus monkeys, and humans and with glycan-binding proteins and antibodies to gather information about the structures of antigenic glycans, which also were analyzed by mass spectrometry. A major glycan antigen targeted by IgG from different infected species is the FLDNF epitope [Fuc␣3GalNAc␤4(Fuc␣3)GlcNAc-R], which is also recognized by the IgG monoclonal antibody F2D2. The FLDNF antigen is expressed by all life stages of the parasite in mammalian hosts, and F2D2 can kill schistosomula in vitro in a complement-dependent manner. Different antisera also recognized other glycan determinants, including core ␤-xylose and highly fucosylated glycans. Thus, the natural shotgun glycan microarray of schistosome eggs is useful in identifying antigenic glycans and in developing new anti-glycan reagents that may have diagnostic applications and contribute to developing new vaccines against schistosomiasis. Schistosomiasis is a major health problem in tropical and subtropical areas where it is endemic, with more than 200 million people actively infected and 800 million at risk of contracting the disease (1-3). Current treatment for disease is limited to the drug praziquantel (4), but cases of drug resistance have been reported (5). Decades of research on schistosomiasis vaccines have yielded only two candidates for clinical trials, and no encouraging results have been published yet (6-9). Thus, there is an urgent need to develop more sensitive diagnostic methods and to identify new vaccine candidates.Recent studies have shown that a major part of the host immune response to infection is directed against carbohydrate (glycan) antigens in glycoproteins and glycolipids (10-17). A wide variety of unusual antigenic determinants include glycans containing the LDN, fucosylated LDN sequences (LDNF, LDN-dF, FLDN, and FLDNF), Lewis X (Le x ), poly-Le x , core ␣3 fucose, and core ␤2 xylose structures (Fig. 1) (11, 14, 17), many of which are expressed by all developmental stages of schistosomes (18). Interestingly, monoclonal antibodies (MAbs) specific to these glycans recognize these antigens on the surface of 3-h-old schistosomula, and some anti-glycan antibodies can mediate killing in vitro in a complement-dependent fashion (18-21). Schistosoma mansoniinfected rhesus monkeys, which are known to self-cure after infection, have IgG to many glycan antigens, including Le x , LDN, LDNF, core fucose, and core xylose determinants, and their sera are effective in complement-mediated cytolysis of cells expressing Le x as well as schistosomulum larvae in ...

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“…Adult worms were obtained at 6 weeks postinfection by manual separation under a light microscope. Eggs were obtained from the liver and purified as previously described (27,28). Briefly, S. japonicuminfected mice were euthanized 6 weeks postinfection, and their livers were removed, cut into pieces, and homogenized with a pestle.…”

Section: Methodsmentioning

confidence: 99%

“…The SWA and SEA were prepared according to previously reported methods (28,29), with minor modifications. Briefly, S. japonicum paired adult worms and purified eggs were washed in phosphate-buffered saline (PBS) five times to reduce contamination by host components.…”

Section: Methodsmentioning

confidence: 99%

Tim-3 Induces Th2-Biased Immunity and Alternative Macrophage Activation during Schistosoma japonicum Infection

et al. 2015

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bT cell immunoglobulin-and mucin-domain-containing molecule 3 (Tim-3) has been regarded as an important regulatory factor in both adaptive and innate immunity. Recently, Tim-3 was reported to be involved in Th2-biased immune responses in mice infected with Schistosoma japonicum, but the exact mechanism behind the involvement of Tim-3 remains unknown. The present study aims to understand the role of Tim-3 in the immune response against S. japonicum infection. Tim-3 expression was determined by flow cytometry, and increased Tim-3 expression was observed on CD4 ؉ and CD8 ؉ T cells, NK1.1 ؉ cells, and CD11b؉ cells from the livers of S. japonicum-infected mice. However, the increased level of Tim-3 was lower in the spleen than in the liver, and no increase in Tim-3 expression was observed on splenic CD8؉ T cells or CD11b Schistosomiasis is a human helminth infection that is estimated to afflict 200 million people worldwide (1). The pathogenesis of schistosomiasis is caused by egg-induced granuloma formation and subsequent fibrosis in hepatic and intestinal tissues, which is believed to be caused by the acquisition and accumulation of immune cells in the affected organs. The immune response that occurs during this process is complicated and poorly understood. During the early stages of infection, a type 1 T-helper-cell (Th1) response is induced by parasite migration and adult worms. As the eggs are released from the mature adult worms, the response is then polarized into a Th2 response 4 to 6 weeks after the initial infection. This is then followed by the development of granulomas around the eggs trapped in the liver. Macrophages surround the deposited eggs and play a pivotal role in the formation of fibrosis (2), since these cells are involved in Th2 development during schistosomiasis (3) and undergo either M1 or M2 activation (4-6). M2 macrophages are essential for host protection via the production of interleukin-10 (IL-10) but simultaneously promote progressive pathology due to granuloma formation (7,8). Although the pathogenesis of schistosomal infection has long been known, the molecules and cells involved in immune triggering against the parasite remain enigmatic.T cell immunoglobulin-and mucin-domain-containing molecule 3 (Tim-3) is an important regulatory factor in both adaptive and innate immunity (9). Tim-3 is preferentially expressed on activated Th1 cells but not Th2 cells (10). After binding to its ligand galectin-9, Tim-3 induces the death of Th1 cells and negatively regulates the Th1 response (11-13). This process plays critical roles in autoimmunity, allergy, viral infection, and transplant tolerance (9). Increased Tim-3 also leads to CD8 ϩ T cell exhaustion, thereby abrogating proliferation, cytotoxicity, and cytokine production during viral infection (14, 15) and acute graft-versushost disease (16). Apart from T cells, Tim-3 is also expressed on a variety of other immune cells, such as natural killer (NK) cells, monocytes, macrophages, and mast cells (17-19). Tim-3 was reported to inhibit NK cell c...

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Schistosomiasis

Cited by 129 publications

References 56 publications

Infection with schistosome parasites in snails leads to increased predation by prawns: implications for human schistosomiasis control

Infection with schistosome parasites in snails leads to increased predation by prawns: implications for human schistosomiasis control

Identification of Antigenic Glycans from Schistosoma mansoni by Using a Shotgun Egg Glycan Microarray

Tim-3 Induces Th2-Biased Immunity and Alternative Macrophage Activation during Schistosoma japonicum Infection

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