sRNA113 regulates Pseudomonas plecoglossicida motility to affect immune response against infection in pearl gentian grouper.

Abstract

Small RNAs (sRNAs) are a class of molecules capable of perceiving environmental changes and exerting post-transcriptional regulation over target gene expression, thereby influencing bacterial virulence and host immune responses. Pseudomonas plecoglossicida is a pathogenic bacterium that poses a significant threat to aquatic animal health. However, the regulatory mechanisms of sRNAs in P. plecoglossicida remain unclear. This study focused on sRNA113, previously identified as a potential regulator of the fliP gene, a key component of the lateral flagellar type III secretion system. To investigate the effects of sRNA113 on P. plecoglossicida virulence, as well as its role in regulating pathogenic processes and host immune responses, mutant strains lacking this sRNA were generated and analyzed. Deletion of sRNA113 resulted in the up-regulation of lateral flagellar type III secretion system-related genes in P. plecoglossicida, which enhanced bacterial swarming motility, biofilm formation, and chemotaxis ability in vitro. In vivo infection experiments with pearl gentian grouper revealed that sRNA113 deletion enhanced the pathogenicity of P. plecoglossicida. This heightened virulence was attributed to the up-regulation of genes associated with the lateral flagellar type III secretion system, resulting in higher bacterial loads within host tissues. This amplification of pathogenic activity intensified tissue damage, disrupted immune responses, and impaired the ability of the host to clear infection, ultimately leading to mortality. These findings underscore the critical role of sRNA113 in regulating the virulence of P. plecoglossicida and its interaction with host immune defenses. This study provides a foundation for further exploration of sRNA-mediated mechanisms in bacterial pathogenesis and host-pathogen interactions, contributing to a deeper understanding of virulence regulation and immune evasion in aquatic pathogens.