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

Abstract

<h4>Introduction</h4>The virulence of <i>Yersinia ruckeri</i>, the causative agent of enteric redmouth disease in salmonids, is influenced by multiple factors, including flagellar gene expression. This study investigates the role of <i>fliC</i> gene expression in the pathogenicity of <i>Y. ruckeri</i> and its impact on the immune response of infected rainbow trout (<i>Oncorhynchus mykiss</i>).<h4>Material and methods</h4>Using two virulent strains differing in <i>fliC</i> 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.<h4>Results</h4>Fish infected with the <i>fliC</i>-repressed strain exhibited more severe symptoms, higher mortality rates and a weaker immune response regardless of infectious dose compared to those infected with the <i>fliC</i>-expressing strain. The lack of an active <i>fliC</i> 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.<h4>Conclusion</h4>These findings clearly demonstrate the dual role of the <i>fliC</i> gene in the pathogenicity of <i>Y. ruckeri</i> and host immune modulation in rainbow trout.