Abstract
We previously reported that the Vibrio vulnificus hemolysin A (VvhA) protein elicited good immune protection and could effectively control V. vulnificus infection in mice. However, its molecular mechanism remains unknown. We hypothesized that hemolysin A induces an immunoprotective response via IL-21 regulation. To demonstrate this, IL-21 expression in mice was regulated by injecting either specific antibodies or rIL-21, and the immune response was evaluated by flow cytometry. Our results suggested that IL-21 enhances immune protection by inducing a T follicular helper cell and germinal center B cell response. We used RNA-seq to explore molecular mechanisms and identified 10 upregulated and 32 downregulated genes involved in IL-21-upregulated protection. Gene Ontology analysis and pathway analysis of the differentially expressed genes were also performed. Our findings indicate that IL-21 can enhance the immune protection effect of the VvhA protein and may serve as a novel strategy for enhancing the immune protection effect of protein vaccines.
Highlights
Vibrio vulnificus (V. vulnificus) is a marine gram-negative bacterium that is responsible for fatal septicemia and necrotizing wound infections through either the ingestion of contaminated seafood or wound infections in humans [1,2,3]
We previously reported that the Vibrio vulnificus hemolysin A (VvhA) protein elicited good immune protection and could effectively control V. vulnificus infection in mice
These data implied that improving the function of IL-21 can enhance the immune protection effect of VvhA protein and reduce the damage caused by V. vulnificus infection in mice
Summary
Vibrio vulnificus (V. vulnificus) is a marine gram-negative bacterium that is responsible for fatal septicemia and necrotizing wound infections through either the ingestion of contaminated seafood or wound infections in humans [1,2,3]. Hemolysin is a very powerful virulence factor of V. vulnificus and is a likely candidate for the pathogenesis of V. vulnificus infections [7]. V. vulnificus hemolysin A (VvhA) toxin has cytolytic and hemolytic activity and is responsible for the death of host cells during the infection [8, 9]. This toxin attaches to the host cell membrane to induce hemolysis by forming small ion permeable pores via colloidal osmotic shock [10, 11]. VvhA may contribute to bacterial invasion from the intestine to the bloodstream and other organs; deletion of VvhA from V. vulnificus has been shown to attenuate its virulence [12]
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