Genomic and Transcriptomic Insights into Cultured Protists
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB79909 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| Other | ||||
| ERR13913812_1.fastq.gz | Fastqsanger.gz | |||
| ERR13913812_2.fastq.gz | Fastqsanger.gz | |||
| ERR13913813_1.fastq.gz | Fastqsanger.gz |
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Project description:Intestinal protists are emerging as key modulators of host immunity and microbial ecology, yet their roles remain poorly defined. Here, we investigated the role of two distinct protists, the amoeba Entamoeba muris, and the parabasalid, Tritrichomonas, to determine how they shape gut immunity in vivo individually and together. Unlike the well-characterized inducer of type 2 immunity, Tritrichomonas, which activates the tuft cell–IL-25–ILC2 circuit in the small intestine, E. muris failed to elicit robust immune responses in the intestine or colon. However, introduction of E. muris into mice naturally colonized by Tritrichomonas spp., or co-infection with E. muris and Tritrichomonas spp. suppressed the Tritrichomonas-induced type-2 response in the small intestine. Fecal and cecal qPCR suggest that E. muris may outcompete Tritrichomonas spp., with reduced protist loads in the cecum and possibly diminished succinate-driven tuft cell activation. We also identified sex-specific differences in the intestinal response to primary Tritrichomonas spp. colonization which have not previously been described. These findings reveal that E. muris can dampen existing type-2 immune circuits without triggering overt inflammation, underscoring its role as an immunomodulatory agent. This work provides a framework for understanding how commensal protists interact within the gut ecosystem and shape mucosal immunity in the absence of pathogenicity.
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Project description:Tissue and microbial cues regulate the abundance and function of CD8+ T cells at barrier sites, yet the impact of specific microbes on their long-term durability remains unclear. Here, we show that the commensal protist Tritrichomonas musculus (T. mu) depletes intestinal CD8+ T cells, particularly tissue resident memory (TRM) cells, through activation of localized type 2 immunity. Colonization with T. mu or administration of its major secreted metabolite, succinate, led to the rapid decline of intestinal CD8+ T cells but left systemic memory T cells unaffected. The purinergic receptor, P2RX7, is highly expressed by intestinal TRMs and chemical antagonism of this receptor markedly restored CD8+ T cells during succinate feeding. Using lymphocytic choriomeningitis virus (LCMV) infection to track antigen-specific CD8+ memory T cells, we found viral-specific CD8+ TRMs repopulate the intestine independent of LCMV reinfection after removal of succinate treatment. These findings highlight how commensal protists and their metabolites reset homeostatic CD8+ T cell carrying capacity through damage-independent stimulation of TRM apoptosis and regulate mucosal memory.
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Project description:The protists genomics RNA-Seq identification, alignment and visualisation pipeline
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Project description:BackgroundLaurel wilt caused by Raffaelea lauricola is a lethal vascular disease of North American members of the Lauraceae plant family. This fungus and its primary ambrosia beetle vector Xyleborus glabratus originated from Asia; however, there is no report of laurel wilt causing widespread mortality on native Lauraceae trees in Asia. To gain insight into why R. lauricola is a tree-killing plant pathogen in North America, we generated and compared high quality draft genome assemblies of R. lauricola and its closely related non-pathogenic species R. aguacate.ResultsRelative to R. aguacate, the R. lauricola genome uniquely encodes several small-secreted proteins that are associated with virulence in other pathogens and is enriched in secondary metabolite biosynthetic clusters, particularly polyketide synthase (PKS), non-ribosomal peptide synthetase (NRPS) and PKS-NRPS anchored gene clusters. The two species also exhibit significant differences in secreted proteins including CAZymes that are associated with polysaccharide binding including the chitin binding CBM50 (LysM) domain. Transcriptomic comparisons of inoculated redbay trees and in vitro-grown fungal cultures further revealed a number of secreted protein genes, secondary metabolite clusters and alternative sulfur uptake and assimilation pathways that are coordinately up-regulated during infection.ConclusionsThrough these comparative analyses we have identified potential adaptations of R. lauricola that may enable it to colonize and cause disease on susceptible hosts. How these adaptations have interacted with co-evolved hosts in Asia, where little to no disease occurs, and non-co-evolved hosts in North America, where lethal wilt occurs, requires additional functional analysis of genes and pathways.
| S-EPMC7441637 | biostudies-literature