Abstract
Aeromonas veronii is a significant pathogen that is capable of infecting humans, animals, and aquatic animals. The type III secretion system (T3SS) is intimately associated with bacterial pathogenicity. The ascO gene is an important core component of T3SS in A. veronii , but its function is still unclear. The ascO gene of A. veronii TH0426 was deleted by using the pRE112 suicide plasmid to study its function. The study results showed that the ability of ∆ ascO to adhere and invade EPC cells was significantly reduced by 1.28 times. The toxicity of the mutant strain Δ ascO to EPC cells was consistently significantly lower than wild‐type strain TH0426 at 1, 2, and 4 h. The LD50 values of ∆ ascO against zebrafish and Carassius auratus ( C. auratus ) were 53 and 15 times that of the wild‐type strain. In addition, the bacterial load of the mutant strain Δ ascO in blood, heart, liver, and spleen was lower than wild‐type strain TH0426. The Hoechst staining showed that the apoptotic degree of EPC cells induced by the mutant strain Δ ascO was lower than that of the wild‐type strain TH0426. Furthermore, real‐time quantitative PCR (RT‐qPCR) analysis revealed lower expression levels of pro‐apoptotic genes (including cytC , cas3 , cas9 , TNF‐α, and IL‐1β) in C. auratus tissues infected with the mutant strain Δ ascO compared to the wild‐type strain TH0426. The results of in vivo and in vitro experiments have shown that ascO gene mutation can reduce the adhesion and toxicity of A. veronii to EPC and reduce the level of apoptosis induced by A. veronii . As a result, these insights will help further elucidate the function of the ascO gene and thus contribute to understanding the pathogenesis of A. veronii .