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Anisakis pegreffii infection of poikilotherm and homeotherm host - keeping it cool makes it better

Anisakiasis is considered one of the most important foodborne parasitic zoonoses, although the nematode cannot complete its life cycle in humans. Generation of -omics data has enabled more versatile approached to study host-parasite interactions. To scrutinise transcriptomic signature of Anisakis pegreffii infective larvae (L3) during migration through a oikilotherm (fish, paratenic host) and homeotherm accidental host(rat, model for human infection), we RNA-sequenced (Illumina) isolated L3, performed a differential analysis of gene expression (DEGs) and calculated the enrichment of GO terms and KEGG pathways within DEGs sets. We also differentiated between transcripts of successfully migrating L3 vs those that were expelled through faeces from the host (non-migrating). The final transcriptome, filtered for transcripts with a detectible coding sequence, resulted in 36, 201 transcripts with predicted ORFs and 4, 016 proteins represented by nearly fulllength transcripts and >80% alignment coverage. Of these, 1, 937 were found ifferentially expressed (FDR < 0.05) in migrating vs. non-migrating L3 in rat, Rattus norvegicus (1, 096 up and 841 down), 484 in sea bass, Dicentrarchus labrax (328 up and 156 down) and 509 were differentially regulated in the two hosts. The largest difference in log2FC between migrating L3 in rat and in sea bass was observed for putative cuticle collagen (CO155) and glucose-6-phosphate exchanger (G6PT1), which were both upregulated in rat and downregulated in sea bass, while the opposite was observed for NADH-dependent flavin oxidoreductase (NADA). In the homeothermic accidental host (rat), Anisakis L3 upregulated ribosome-related genes, cell division, cuticle constituents, oxidative phosphorylation, probably in an unsuccessful effort to moult to the next developmental stage. Contrary, in the paratenic poikilotherm host (fish), L3 moderately upregulated or silenced the main metabolic pathways, preparing for dormancy by triggering autophagy and longevity pathways. We hypothesise that the failure of L3 to survive in the accidental host is a result of metabolic/ energy exhaustion that occurs from undetermined migration towards a suitable niche that is never to be achieved, additionally stimulated by host homeothermy. In the poikilotherm paratenic host, moderately upregulated or silenced metabolism serves to enable larvae to prepare for paratenesis, warranting their survival.

Anisakis ; paratenic host ; accidental host ; anisakiasis ; transcriptomics

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