Immunological Studies in Human Schistosomiasis

Capron, Moníque; Camus, Daniel; Carlier, Yves; Figueiredo, J. F. M.; Càpron, André

doi:10.4269/ajtmh.1977.26.248

Cited by 13 publications

(1 citation statement)

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“…This model is consistent with previous observations that show the importance of antibodies and exposing inner parasite tissues for a successful immune response for eliminating schistosomes ( 51 – 55 ). In vitro studies have shown that the addition of antibodies is necessary for effector cells (e.g., eosinophils) to kill schistosomula ( 51 – 53 ). Similarly, in vivo, praziquantel-treated adult schistosomes were only killed when immune cells and antibodies gained access to inner parasite tissues through the damaged tegument ( 54 , 55 ).…”

Section: Discussionsupporting

confidence: 93%

The esophageal gland mediates host immune evasion by the human parasiteSchistosoma mansoni

Lee

Chong

Newmark

2020

Proc. Natl. Acad. Sci. U.S.A.

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Schistosomes are parasitic flatworms that cause schistosomiasis, a neglected tropical disease affecting over 200 million people. Schistosomes develop multiple body plans while navigating their complex life cycle, which involves two different hosts: a mammalian definitive host and a molluscan intermediate host. Their survival and propagation depend upon proliferation and differentiation of stem cells necessary for parasite homeostasis and reproduction. Infective larvae released from snails carry a handful of stem cells that serve as the likely source of new tissues as the parasite adapts to life inside the mammalian host; however, the role of these stem cells during this critical life cycle stage remains unclear. Here, we characterize stem cell fates during early intramammalian development. Surprisingly, we find that the esophageal gland, an accessory organ of the digestive tract, develops before the rest of the digestive system is formed and blood feeding is initiated, suggesting a role in processes beyond nutrient uptake. To explore such a role, we examine schistosomes that lack the esophageal gland due to knockdown of a forkhead-box transcription factor, Sm-foxA, which blocks development and maintenance of the esophageal gland, without affecting the development of other somatic tissues. Intriguingly, schistosomes lacking the esophageal gland die after transplantation into naive mice, but survive in immunodeficient mice lacking B cells. We show that parasites lacking the esophageal gland are unable to lyse ingested immune cells within the esophagus before passing them into the gut. These results unveil an immune-evasion mechanism mediated by the esophageal gland, which is essential for schistosome survival and pathogenesis.

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Section: Discussionsupporting

confidence: 93%

The esophageal gland mediates host immune evasion by the human parasiteSchistosoma mansoni

Lee

Chong

Newmark

2020

Proc. Natl. Acad. Sci. U.S.A.

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Complement regulation on the surface of cultured schistosomula and adult worms of Schistosoma mansoni

et al. 1990

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Cercaria and freshly prepared schistosomula of Schistosoma mansoni are highly sensitive to complement. However, early in their maturation, the schistosomula become resistant to complement killing. This conversion is preceded by a rapid and massive release of several acetabular proteases and of the glycocalyx coat. Thus, shedding of the glycocalyx which is a major immunogen and a strong activator of the alternative pathway of complement permits the parasite to escape immune damage. Mechanically transformed schistosomula, which were cultured in a defined synthetic medium and developed complement resistance, could be converted by proteolysis to complement sensitivity. Trypsin and pronase markedly increased the susceptibility of cultured schistosomula to complement. The trypsin-induced complement sensitivity persisted for at least 19 h without recovery of resistance. Similar treatment with trypsin produced complete killing of adult worms by complement in absence of antibodies. Efficient killing was obtained with normal human serum (NHS), with normal guinea pig serum (GpS), and with C4-depleted HS and C4-deficient GpS indicating that the killing was mediated by the cytolytic alternative pathway of complement. Larger quantities of C3b with intact alpha' chain could be demonstrated on trypsin-treated than on non-treated schistosomula. Antibodies which were raised in rabbits by immunization with the trypsin-released material bound to cultured (non-treated) schistosomula and to adult worms, and induced their killing in GpS and C4-deficient GpS. These results suggest that following release of the glycocalyx, the transforming schistosomula of S. mansoni spontaneously express a complement regulatory protein(s). A similar regulator is postulated to be present on the surface of adult worms. Such regulatory molecules may serve as good targets for immunotherapy, since antibodies directed to them will inhibit their regulatory activity and thus potentiate in vivo the lytic action of complement.

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Immunity to Schistosomiasis: in vitro versus in vivo Models

McLaren¹,

Smithers²

1982

Animal Models in Parasitology

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Immunological Studies in Human Schistosomiasis

Cited by 13 publications

References 0 publications

The esophageal gland mediates host immune evasion by the human parasiteSchistosoma mansoni

The esophageal gland mediates host immune evasion by the human parasiteSchistosoma mansoni

Complement regulation on the surface of cultured schistosomula and adult worms of Schistosoma mansoni

Immunity to Schistosomiasis: in vitro versus in vivo Models

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