Repression of the fliC gene as an immune evasion strategy in Yersinia ruckeri infection of rainbow trout (Oncorhynchus mykiss).

Abstract

Introduction: The virulence of Yersinia ruckeri, the causative agent of enteric redmouth disease in salmonids, is influenced by multiple factors, including flagellar gene expression. This study investigates the role of fliC gene expression in the pathogenicity of Y. ruckeri and its impact on the immune response of infected rainbow trout (Oncorhynchus mykiss).

Material and methods: Using two virulent strains differing in fliC expression, clinical symptoms, mortality rates and key immune parameters were evaluated. Ninety farmed rainbow trout with average body weight of 110.5 ± 24.1 g and average length of 20.7 ± 1.9 cm were used. Allocation was made of 10 fish each to a control group, a low-dose group challenged with one strain, a high-dose group challenged with that strain, and low- and high-dose groups challenged with the second strain, and each challenge group was duplicated.

Results: Fish infected with the fliC-repressed strain exhibited more severe symptoms, higher mortality rates and a weaker immune response regardless of infectious dose compared to those infected with the fliC-expressing strain. The lack of an active fliC gene was associated with a lower gammaglobulin level, decreased respiratory burst and suppressed T-cell proliferation. However, increased potential killing activity was noted for that strain.

Conclusion: These findings clearly demonstrate the dual role of the fliC gene in the pathogenicity of Y. ruckeri and host immune modulation in rainbow trout.