Abstract | Shore crabs (Carcinus maenas) act as mobile reservoirs of microparasites, including pathogenic dinoflagelleates belonging to the genus Hematodinium. Despite the widespread prevalence and documented seasonality of Hematodinium sp. infection dynamics in ∼ 50 species of decapod crustaceans globally, there is a knowledge gap regarding host-pathogen antibiosis. How does Hematodinium avoid the host’s immune defences? Herein, we profiled the haemolymph of Hematodinium-positive and Hematodinium-negative crabs for extracellular vesicles (EVs; a proxy for cellular communication), alongside proteomic signatures for post-translational citrullination/deimination performed by arginine deiminases, which can infer a pathologic state. Aditionally, we used 16S rRNA metabarcoding to monitor the haemolymph bacteriome of parasitised and control shore crabs. Circulating EV numbers in parasitized crab haemolymph were reduced significantly, accompanied by smaller EV modal size profiles when compared to Hematodinium-negative controls. Notably, Down syndrome cell adhesion molecule (DSCAM) and nitric oxide synthase were two factors identified as citrullinated in parasitsed crabs. Patent Hematodinium sp. infection did not appear to coincide with haemolymph dysbiosis (bacterial richness or diversity), despite the gross accumulation of the parasite in liquid and solid tissues. These data enhance our understanding of Hematodinium-crustacean pathosystems. |
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