Int J Biol Macromol 2025 Jun 23;315Pt 2:144606. doi: 10.1016/j.ijbiomac.2025.144606.

Vibrio splendidus type VI secretion system hemolysin-coregulated protein inhibits the inflammatory response of Apostichopus japonicus by interacting with major yolk protein 1.

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Consistent with inflammation being an important host defense mechanism, bacterial pathogens have evolved strategies to evade or paralyze the inflammation system. Research indicates that the type VI secretion system (T6SS) is closely associated with the pathogenicity of bacteria. However, it remains unclear whether T6SS protein regulates coelomocyte inflammation during Vibrio splendidus infection and what the underlying molecular mechanisms are. In the current study, we demonstrated that hemolysin-coregulated protein (VsHcp) was significantly upregulated upon stimulation by Apostichopus japonicus coelomic fluid and was localized in the coelomocytes of A. japonicus. The VsHcp deletion mutant (ΔVsHcp) was constructed to investigate whether it regulates the immune pathway of A. japonicus. Compared to the wild-type strain treatment group, the mortality rate of the knockout strain was significantly reduced. Immunofluorescence analysis showed that VsHcp was secreted into the coelomocytes of sea cucumbers through the T6SS. The deletion of VsHcp exacerbated the inflammatory response induced by V. splendidus and activated inflammatory factors in the NF-κB pathway. Furthermore, the GST-pull down assays revealed that VsHcp protein interacted with major yolk protein 1 of A. japonicus (AjMYP1). These findings indicate a V. splendidus T6SS-based mechanism that negatively regulates inflammation by interacting with AjMYP1 protein.

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