Toll-crustin signaling pathway is activated in the Eriocheir sinensis with hepatopancreatic necrosis disease (HPND)

Abstract

The occurrence of hepatopancreatic necrosis disease (HPND) puts pressure on the healthy aquaculture and development of Chinese mitten crab, Eriocheir sinensis. Research on the mechanism of innate immunity regulation in crabs with HPND is limited. We studied the effects of HPND on the expression of Toll receptor and crustin gene, as well as the relationship between Toll and the synthesis of crustin in E. sinensis. The full-length cDNA and genome structure of six Tolls (EsToll1–6) and five crustins (EsCru1–5) were acquired by gene cloning. The genome of EsToll1–6 can be divided into three types, namely, typical, intronless, and vertebrate-like Tolls. Predicted protein domains showed that all the Tolls and crustins contained the conserved Toll-interleukin1-resistance (TIR) and whey acidic protein (WAP) domain, respectively. Evolutionary analysis results displayed that EsToll1–6 and EsCru1–5 clustered with other Toll receptors and crustin proteins from crustaceans, respectively. EsToll3–6 and EsCru3–5 were widely distributed in multiple immune tissues. EsToll1–5 and EsCru1,2,4,5 expressions in the intestine of crabs with HPND significantly increased. The knockdown of EsToll1–6 could evidently decrease the expressions of different crustins that were positively regulated by HPND. The Toll-crustin signaling pathway was activated in diseased crabs, which may be related to the starvation caused by HPND. Crabs in a state of starvation due to HPND activate their innate immune system. This may be a strategy for the body to protect itself against microbial infection. Our study provides new insights for HPND research.