Molecular context of Schistosoma mansoni transmission in the molluscan environments: A mini-review

Famakinde, Damilare O

doi:10.1016/j.actatropica.2017.07.021

Cited by 12 publications

(9 citation statements)

References 86 publications

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“…A major physiological determinant of snail resistance/susceptibility to infections, which is also under genetic influence, is the snail internal defense system (IDS). The IDS comprises the cellular elements (hemocytes) and the humoral (plasma) factors of the hemolymph that work independently or in concert to recognize, encapsulate, kill, and clear intruding trematodes [ 6 , 54 , 55 , 56 ]. Establishment of the B. glabrata embryonic ( Bg e) cell line in 1976 [ 57 ] provided an enabling avenue for investigators to delve into the molecular and cellular aspects of the complex snail immune functions against schistosomes by using an in vitro culture model, rather than using the whole intact animal, which could have resulted in a rudimentary understanding of the complex biological events.…”

Section: Biology Of Snail Resistance/susceptibility To Smentioning

confidence: 99%

“…The eggs that reach the vectors’ freshwater habitats hatch and release the enclosed miracidia larvae, which swim actively to locate and infect their snail vectors. A miracidium that successfully infects a susceptible vector undergoes intramolluscan polyembryonic development to produce thousands of actively-swimming tailed cercariae larvae that emerge continuously from the snail host for the rest of the its lifetime (spanning months) [ 3 , 4 , 5 , 6 ]. Human infection with schistosomes is acquired through skin contact with, and subsequent penetration by, the cercariae during recreational, domestic, or occupational activities with contaminated water [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

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Treading the Path towards Genetic Control of Snail Resistance to Schistosome Infection

Famakinde¹

2018

TropicalMed

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Schistosomiasis remains the most important tropical snail-borne trematodiasis that threatens many millions of human lives. In achieving schistosomiasis elimination targets, sustainable control of the snail vectors represents a logical approach. Nonetheless, the ineffectiveness of the present snail control interventions emphasizes the need to develop new complementary strategies to ensure more effective control outcomes. Accordingly, the use of genetic techniques aimed at driving resistance traits into natural vector populations has been put forward as a promising tool for integrated snail control. Leveraging the Biomphalaria-Schistosoma model system, studies unraveling the complexities of the vector biology and those exploring the molecular basis of snail resistance to schistosome infection have been expanding in various breadths, generating many significant discoveries, and raising the hope for future breakthroughs. This review provides a compendium of relevant findings, and without neglecting the current existing gaps and potential future challenges, discusses how a transgenic snail approach may be adapted and harnessed to control human schistosomiasis.

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Section: Biology Of Snail Resistance/susceptibility To Smentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Treading the Path towards Genetic Control of Snail Resistance to Schistosome Infection

Famakinde¹

2018

TropicalMed

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“…The resistance phenotype is underpinned by a complex genetic trait, where the schistosome larva fails to develop as the consequence of innate and cellular immune responses. Hemocytes of resistant snails encapsulate and destroy the sporocyst [11][12][13][14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Diminished adherence of Biomphalaria glabrata embryonic cell line to sporocysts of Schistosoma mansoni following programmed knockout of the allograft inflammatory factor

et al. 2020

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Background Larval development in an intermediate host gastropod snail of the genus Biomphalaria is an obligatory component of the life-cycle of Schistosoma mansoni. Understanding of the mechanism(s) of host defense may hasten the development of tools that block transmission of schistosomiasis. The allograft inflammatory factor 1, AIF, which is evolutionarily conserved and expressed in phagocytes, is a marker of macrophage activation in both mammals and invertebrates. AIF enhances cell proliferation and migration. The embryonic cell line, termed Bge, from Biomphalaria glabrata is a versatile resource for investigation of the snail-schistosome relationship since Bge exhibits a hemocyte-like phenotype. Hemocytes perform central roles in innate and cellular immunity in gastropods and in some cases can kill the parasite. However, the Bge cells do not kill the parasite in vitro. Methods Bge cells were transfected by electroporation with plasmid pCas-BgAIFx4, encoding the Cas9 nuclease and a guide RNA specific for exon 4 of the B. glabrata AIF (BgAIF) gene. Transcript levels for Cas9 and for BgAIF were monitored by reverse-transcription-PCR and, in parallel, adhesion of gene-edited Bge cells during co-culture with of schistosome sporocysts was assessed. Results Gene knockout manipulation induced gene-disrupting indels, frequently 1–2 bp insertions and/or 8–30 bp deletions, at the programmed target site; a range from 9 to 17% of the copies of the BgAIF gene in the Bge population of cells were mutated. Transcript levels for BgAIF were reduced by up to 73% (49.5 ± 20.2% SD, P ≤ 0.05, n = 12). Adherence by BgAIF gene-edited (ΔBgAIF) Bge to sporocysts diminished in comparison to wild type cells, although cell morphology did not change. Specifically, as scored by a semi-quantitative cell adherence index (CAI), fewer ΔBgAIF than control wild type cells adhered to sporocysts; control CAI, 2.66 ± 0.10, ΔBgAIF, 2.30 ± 0.22 (P ≤ 0.01). Conclusions The findings supported the hypothesis that BgAIF plays a role in the adherence of B. glabrata hemocytes to sporocysts during schistosome infection in vitro. This demonstration of the activity of programmed gene editing will enable functional genomics approaches using CRISPR/Cas9 to investigate additional components of the snail-schistosome host-parasite relationship.

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“…Hemocytes of resistant snails encapsulate and destroy the sporocyst [11][12][13][14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Diminished Adherence of Biomphalaria Glabrata Embryonic Cell Line to Sporocysts of Schistosoma Mansoni Following Programmed Knockout of the Allograft Inflammatory Factor

Coelho

Rodpai

Miller

et al. 2020

Preprint

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The development of the larval stage of Schistosoma mansoni in an intermediate host snail of the genus Biomphalaria is an obligatory component of the life cycle. Enhanced understanding of the mechanism(s) of host defense in the snail may hasten the development of tools that block transmission of schistosomiasis. The B. glabrata embryonic cell line, termed the Bge line, is a versatile resource for investigation of the snail-schistosome relationship. A key attribute of the Bge cell is the hemocyte-like phenotype, given the central role of the snail hemocyte in innate and cellular immunity. The allograft inflammatory factor 1, AIF, is evolutionarily conserved, typically is expressed in phagocytes and granular leukocytes, is a marker of macrophage activation in mammals and in invertebrates, and enhances cell proliferation and migration. AIF is highly expressed in strains of B. glabrata resistant S. mansoni infection in comparison with susceptible strains of the snail. We hypothesized that BgAIF may play a role in hemocyte proliferation, adhesion and/or migration after exposure of the snail to schistosomes. CRISPR/Cas gene knockout of the BgAIF gene in Bge cells was undertaken to investigate the hypothesis. Gene knockout manipulation induced gene-disrupting indels, frequently 1–2 bp insertions and/or 8–30 bp deletions, at the programmed target site; a range from 9 to 17% of BgAIF genes were mutated during 12 replicate experiments, and transcript levels for BgAIF were significantly reduced by up to 73% (range, 26 to 73%, mean 49.5 ± 20.2% S.D, n = 12) when monitored for up to nine days following the gene-editing manipulation. The adherence to sporocyst of BgAIF gene-edited (ΔBgAIF) Bge cells was significantly diminished in comparison to wild type cells, even though cell morphology did not differ between ΔBgAIF treatment and control groups of Bge cells. A Bge cell adherence index (CAI) to individual sporocysts was observed at 2.66 ± 0.10 for control and 2.30 ± 0.22 in ΔBgAIF cells (P < 0.05), revealing that ΔBgAIF cells were significantly less adherent than wild type Bge cells to primary sporocysts. The findings supported the hypothesis that BgAIF plays a role in the adherence of B. glabrata hemocytes to sporocysts during schistosome infection.

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Molecular context of Schistosoma mansoni transmission in the molluscan environments: A mini-review

Cited by 12 publications

References 86 publications

Treading the Path towards Genetic Control of Snail Resistance to Schistosome Infection

Treading the Path towards Genetic Control of Snail Resistance to Schistosome Infection

Diminished adherence of Biomphalaria glabrata embryonic cell line to sporocysts of Schistosoma mansoni following programmed knockout of the allograft inflammatory factor

Diminished Adherence of Biomphalaria Glabrata Embryonic Cell Line to Sporocysts of Schistosoma Mansoni Following Programmed Knockout of the Allograft Inflammatory Factor

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