Submitted to: Fish and Shellfish Immunology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 5/31/2010
Publication Date: 6/8/2010
Citation: Wiens, G.D., Vallejo, R.L. 2010. Temporal and pathogen-load dependent changes in rainbow trout (Oncorhynchus mykiss) immune response traits following challenge with biotype 2 Yersinia ruckeri. Fish and Shellfish Immunology. doi:10.1016/j.fsi.2010.06.010 29:639-647. Interpretive Summary: Yersinia ruckeri is the bacterium that causes enteric redmouth disease (ERM) of trout and salmon. Recently, an increase in ERM outbreaks have been reported in the United Kingdom, Spain and the United States that are caused by biotype 2 strains. Biotype 2 strains are defined by the loss of a protein, flagellin, that helps that bacteria swim and is also thought to provoke a strong immune response. Herein, we characterized the rainbow trout immune response following experimental infection with biotype 2 strain YRNC10. We report that fish still produce a strong immune response demonstrating that recognition of flagellin is not required to initiate immune signaling. We observed that following infection, trout produce high levels of serum amyloid A messenger RNA and that gene expression is correlated with increased spleen weight. We suggest that measuring serum amyloid A gene expression and spleen size are effective surrogate markers for predicting rainbow trout health and immunological function.
Technical Abstract: Rainbow trout infected with Yersinia ruckeri, the causative agent of enteric redmouth disease (ERM), produce a pro-inflammatory and acute-phase response attributed in part to the innate recognition of bacterial-produced flagellin. Recently, variants of Yersinia ruckeri have been identified that lack flagella and associated motility. These strains are classified as biotype 2 (BT2) Y. ruckeri and these are considered an emerging problem in salmonid aquaculture. Little is known about the salmonid immune response to these variants. Herein, we report temporal and quantitative changes in rainbow trout immune response parameters following a primary challenge with BT2 Y. ruckeri strain YRNC10. Fish were injection-challenged with ten-fold dilutions of viable bacteria and sampled on days 1, 3, 5 and 7 post-challenge. TNF'1 and IL1-'1 transcripts were increased by day 1 post-challenge, and on days 3, 5 and 7 maximal gene transcript up-regulation occurred at a threshold of ~64 to 256 CFU per mg spleen tissue. Infection induced robust SAA gene up-regulation that was significantly correlated with increased gene expression of IL-1'1 (r=0.81, P<0.0001) and TNF'1 (r=0.55, P<0.0001). Yersinia ruckeri infection induced modest changes in INF' and Mx-1 gene transcript abundance at intermediate or high challenge doses and the expression patterns of both genes were positively correlated with pro-inflammatory gene and acute-phase gene transcription patterns. TNF superfamily 13b (BAFF) gene expression was significantly down-regulated in response to infection on days 3, 5 and 7 at the highest challenge doses. The spleen somatic index was significantly increased on days 3, 5 and 7 post-infection and positively correlated with spleen colony forming units and abundance of gene transcripts SAA, TNF'1, and IL1-'1. In summary, rainbow trout had a strong innate response following challenge with BT2 Y. ruckeri strain YRNC10 indicating that flagellin expression is not required for production of a robust pro-inflammatory and acute-phase gene transcription response. This study further supports the use of SAA transcript abundance and spleen somatic index as general measures of immunological status and fish health.