Teleost fish express three different immunoglobulin isotypes: IgM, IgD and the teleost specific IgT, which is attributed a more mucosal role similar to mammalian IgA. In this study, we describe the complete sequence of gilthead sea bream IgM and IgT in both, their soluble (s) and membrane bound (m) forms and study their differential expression in different tissues and upon infections of different etiology, vaccination and dietary interventions. Gilthead sea bream IgM and IgT show the prototypical structure known for teleost and, while sIgM was the overall highest expressed isoform, mIgT was highest expressed in mucosal tissues such as gills and intestine. IgM and IgT were differentially regulated upon infection. IgT was highly upregulated locally upon infection with the intestinal parasite Enteromyxum leei or systemically after Nodavirus infection. Long-term intestinal parasitic infections increased the serum titer of both isotypes. Mucosal vaccination against Photobacterium damselae subsp. piscicida finely regulated the Ig response inducing a systemic increase of IgM titers in serum and a local IgT response in skin mucus when animals were exposed to the bacterial pathogen by bath challenge. Interestingly, when fish were fed for a long term with plant-based diets, the significant upregulation of sIgT observed in parasite infected intestines and head kidneys of control fed fish was completely inhibited. Fish fed plant-based diets also presented a worse disease outcome reflecting the importance of this immunoglobulin in the maintenance of intestinal health. All these results corroborate the mucosal role of IgT and emphasize the importance of a finely tuned regulation of Ig isotypes upon infection, which could be of special interest in vaccination studies. They also highlight the importance of the dietary conditions as significant regulators of the immune response and disease resistance

This work has been carried out with financial support from by the Spanish MINECO under projects AGL2013-48560-R to JP-S and AS-B and AGL2014-51773-C3-3-R to EG-C. Additional funding was provided by the European Union, through the Horizon H2020 research and innovation program under grant agreement 634429 (ParaFishControl) and through the FP7 under grant 311993 (TargetFish).

Trabajo presentado en la 18th International Conference on Diseases of Fish and Shellfish, celebrada en Belfast, del 4 al 8 de septiembre de 2017

Peer reviewed