Hemolymph and transcriptome analysis to understand innate immune responses to hypoxia in Pacific abalone.

Hypoxia was thought to inhibit immune responses, causing severe mortality to marine organisms. The Pacific abalone, Haliotis discus hannai, is the most widely cultured abalone species in China, but suffering from "summer mortality" in which hypoxia has been one of the main reasons. The effect of hypoxia exposure on immune responses in H. discus hannai was investigated, including cellular immune response using flow cytometry and transcriptome profiles. The influence of hypoxia treatment on the total hemocyte count (THC) of H. discus hannai was rather limited but the hemocyte survival rate of abalone increased during 48 h exposure. There was an initial rise in the production of phagocytes and reactive oxygen species (ROS) shortly (3 h) after hypoxic stimulation, but finally decreased after 48 h. This indicates that hypoxia inhibited redox activity of abalone. RNA-seq studies of gill tissues also revealed immune response mechanism in abalone after 24 h of hypoxia. Totally 954 differentially expressed genes (DEGs) were detected under different degrees of deoxygenation. Though oxidation-reduction turbulence was a result of both up- and down-regulated DEGs, cell death/apoptosis induction resulted from up-regulated DEGs, whilst DNA metabolic and immunity suppression resulted from down-regulated DEGs. In summary, our data provides evidence that deoxygenation greatly affects abalone immunity, probably making it more vulnerable. The present study also lays the foundation for further research in hypoxia-associated conditions in abalone aquaculture.

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