Recently, Professor Xu Tianjun’s Team at SHOU has discovered a new mechanism by which Vibrio harveyi escapes host immunity. This result has been published on iScience, a sub-journal of the Cell, under the title of ACKR4a induces autophagy to block NF-κB signaling and apoptosis to facilitate Vibrio harveyi infection (DOI: 10.1016/j.isci.2023.106105). Professor Xu Tianjun is the corresponding author of this paper, and post-doctor Chen Ya is the first author. This study elucidated a new mechanism by which Vibrio harveyi evaded host immunity by hijacking host autophagy.

Fulminant vibriosis, one of the most serious diseases threatening aquaculture, can cause the death of a large number of infected fish, shrimp, and shellfish. As a serious pathogen in aquatic animals, Vibrio harveyi can induce muscle necrosis, fin rotting, liver and spleen injury, and other life-threatening symptoms in infected fish, causing huge economic losses to the aquaculture industry. Therefore, it is of great significance to explore the way and mechanism by which Vibrio harveyi escapes host immunity during infection.

In this study, the authors found that, after infecting the host, Vibrio harveyi employs host transcription factor AP-1 to promote the expression of ACKR4a, a member of the atypical chemokine receptor family. ACKR4a then forms complexes with Beclin-1 and MyD88 separately to induce autophagy, and transports MyD88 to the lysosome to promote degradation, thereby reducing the intensity of NF-κB pathway-mediated inflammatory responses. On the other hand, ACKR4a-induced autophagy blocks early apoptosis signals by inhibiting caspase8, thereby promoting the colonization and replication of the pathogen in the host. This study demonstrated that Vibrio harveyi can “hijack” host autophagy and destroy TLR-mediated immune and apoptosis signals to escape host immunity, suggesting that Vibrio harveyi has evolved a resistance to fish immunity. This study provided a therapeutic target for the immune prevention and control of bacterial diseases in fish.