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PubMed2025

The structural features and immunological role of biomphalysins in the snail Biomphalaria glabrata.

Biomphalysins are β-Pore Forming Toxins (β-PFT) identified in the planorbid Biomphalaria glabrata that belong to the aerolysin-like protein family. Despite potentially diverse biochemical activities, very few eukaryotic aerolysin-related proteins have been extensively studied. Most of the data refers to their discovery in genomes or to transcriptional activity. The involvement of biomphalysins in the immune response of Biomphalaria glabrata has been studied previously, especially regarding biomphalysin 1, which can bind and kill Schistosoma mansoni mother sporocysts. However, the repartition of biomphalysin 1 protein in B. glabrata has yet to be defined. The transcriptional behavior of the 22 other biomphalysin genes following immune challenge also remains uncharacterized. Therefore, herein, we investigate for the first time the tissular distribution of biomphalysin 1 (and 2) in B. glabrata by histological and cytological analyses through immunofluorescence approaches, notably unveiling unexpected tissue location that are involved in biomphalysin 1 synthesis. Structural predictions of the 23 members of the family have been updated using predictions based on aminoacyl spatial pair representation (AlphaFold2), highlighting unique features of the small lobe. In addition, mass spectrometry-based proteomic data more precisely predicted the regions of post-translational cleavage of biomphalysin 1. Transcriptional activity of the biomphalysin genes was explored, after which the plasmatic presence of the biomphalysin proteins was investigated in naive and S. mansoni-infected snails. The ability of native biomphalysin 1 (and 2) to bind several cell types was also investigated and correlated with the lytic ability of plasma toward the exposed cells, highlighting the central role occupied by biomphalysin 1 (and 2) in the humoral immunity of B. glabrata.

Biomphalaria↗

PubMed2026

Epigenetic and metabolic reprogramming of innate immune cells establishes immunological memory in the Schistosomiasis vector snail Biomphalaria glabrata.

Innate immune memory enables non-vertebrates to mount faster and more effective immune responses upon re-exposure to a previously encountered pathogen, yet its cellular and molecular bases remain poorly understood. The freshwater snail Biomphalaria glabrata, intermediate host of the human parasite Schistosoma mansoni, provides a powerful model to investigate this phenomenon. Here, we show that innate immune memory in B. glabrata is carried by hemocytes and relies on profound metabolic and epigenetic reprogramming initiated during primary infection. Using an integrative multi-omics approach combining transcriptomics, chromatin accessibility profiling, whole-genome bisulfite sequencing and targeted metabolomics, we reveal that the first parasite encounter induces a stable rewiring of hemocyte metabolism and chromatin landscape. This reprogramming primes hemocytes for a massive and rapid transcriptional response upon secondary challenge, characterized by an immune shift toward highly specific humoral effector pathways. Metabolic analyses demonstrate an early switch toward aerobic glycolysis, altered tricarboxylic acid cycle activity and amino acid metabolism, consistent with a Warburg-like metabolic state previously described in vertebrate trained immunity. Notably, metabolic and epigenetic remodeling occurs primarily during the primary infection and remains stable upon secondary exposure, suggesting that immune memory is encoded prior to pathogen re-encounter. Together, our results identify conserved metabolic and epigenetic mechanisms underlying innate immune memory in a non-vertebrate host and provide direct evidence that hemocyte-mediated innate immune memory in B. glabrata shares core features with trained immunity described in vertebrates.

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PubMed2026

Snail immunity to schistosomes: insights from omics studies.

Schistosomiasis is a serious public health concern, with transmission facilitated by a small number of freshwater snail intermediate host species. Infection outcomes vary greatly across the primary vector genera, Biomphalaria (for Schistosoma mansoni), Bulinus (for S. haematobium), and Oncomelania (for S. japonicum), even within species, ranging from full resistance to high compatibility. Omics methods have altered this field by correlating host genotype, baseline immunological status, and time-resolved responses to whether invading miracidia are eliminated or develop sporocysts. Evidence from genomes, transcriptomics, proteomics, and epigenomics suggests that resistance is frequently primed prior to exposure. However, the clearest divergence between resistant and susceptible trajectories occurs during a small early window (<12-48 h) after penetration. During this time, recognition, hemocyte recruitment, and soluble effector deployment either come together quickly or are delayed and guided by parasite-derived modulators. Established infections cause the host to adapt to chronic conditions through immune regulation, metabolic reprogramming, tissue and neuroendocrine remodeling, microbiome modification, and parasite castration. Comparative genomics reveals that each vector genus has evolved its own immunogenomic profile, which includes lineage-specific expansions of recognition and effector gene families. Together, these findings can help with field surveillance and intervention by providing molecular compatibility markers, functional tools for testing candidate genes, and tactics that target parasite-derived immune modulators. Integrated multi-omics approaches are a top priority, yet they are still limited in snail vectors compared to other disease vector systems.

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