engleski

Expression of proinflammatory cytokines IL-1β, TNFα1 and TNFα2 induced by PAMPs and gill parasitic infections in the Atlantic bluefin tuna (Thunnus thynnus) peripheral blood leukocytes and gills

Parasites infecting vascularised tissues, especially gills, are in general quickly detected by both locally secreted and circulating immunity components, causing stronger or weaker inflammatory reaction. Atlantic bluefin tuna Thunnus thynnus is one of the most valuable aquaculture species in the Mediterranean, and interestingly, no economically threatening parasitoses have been reported in adult fish in the Adriatic or Mediterranean aquaculture. Moreover, a decrease in parasite populations is usually observed by the end of the rearing cycle. In order to shed the light on the immunity mechanisms underlying Atlantic bluefin tuna reactions against different pathogen types (bacteria, viruses, parasites) we studied expression profiles of three major cytokines ; IL-1β, TNFα1 and TNFα2 in three different scenarios: 1) in peripheral blood leukocytes (PBL) during in vitro stimulation with lipopolysaccharid (LPS) and polyinosinicpolycytidylic acid (Poly I:C) mimicking bacterial and viral pathogens ; 2) in PBL during in vitro stimulation with didymozoid D. katsuwonicola (Digenea) and siphonostomatoid P. appendiculatus (Copepoda) antigens ; and 3) at the site of D. katsuwonicola and P. appendiculatus parasitation. It resulted that the Atlantic bluefin tuna IL-1β and TNFα2 were induced in LPS/Poly I:C-stimulated PBLs and PBLs treated by parasite-derived antigens, as well as in parasites infected gills. Induction of Atlantic bluefin tuna pro-inflammatory cytokines IL-1β and TNFα2 by PAMPs, D. katsuwonicola- and P. appendiculatus-derived antigens, as well as during natural infection of two parasites, suggests they play an important role in inflammation and host defence against wide array of pathogens, in contrast to TNFα1. Targets' expressions in general followed congruent pattern in parasites TA-stimulated PBL (in vitro model) and in host tissue (in vivo model), diverging only in respect to parasite species.

inflammation; host defence; gene expression

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