Infection of rainbow trout with the parasitic ciliate Ichthyopthirius multifiliis induces differential responses in gills, skin and spleen. A controlled experimental infection was performed and expression of immune-relevant genes in skin, gills, and spleen were recorded by qPCR at day 1 and 8 after parasite exposure. Infection induced a marked reaction involving regulation of innate and adaptive immune genes in rainbow trout at day 8 post-infection. The expression level of a total of 22 out of 24 investigated genes was significantly higher in gills compared to skin reflecting the more sensitive and delicate structure of gills. Especially pro-inflammatory cytokines IL-6, IL-17 C1, regulatory cytokines IL-4/13A, IL-10, TGFβ, complement factor C5, chemokines CK10, CK12, acute phase proteins (precerebellin, hepcidin) and immunoglobulins (IgM, IgT) displayed differential expression levels. The spleen, a central immune organ with no trace of the parasite, showed elevated expression of IgM, IgT, complement factor C5 and chemokine CK10 (compared to skin and gills directly exposed to the parasite), indicating an interaction between the infected surface sites and central immune organs. This communication could be mediated by chemokines CK10 and CK12 and cytokine IL-4/13A and may at least partly explain the establishment of a systemic response in rainbow trout against the parasite.

Third-stage larvae of the anisakid nematode Contracaecum osculatum infecting cod (Gadus morhua) liver elicit a host immune response involving both innate and adaptive factors, but the reactions differ between liver and spleen. Inflammatory reactions occur in both liver and spleen, but a series of immune effector genes are downregulated in liver infected with nematodes whereas these genes in spleen from the same fish are upregulated. A series of novel primer and probe sets targeting cod immune responses were developed and applied in a real-time quantitative polymerase chain reaction set-up to measure the expression of immune-relevant genes in liver and spleen of infected and uninfected cod. In infected liver, 12 of 23 genes were regulated. Genes encoding cytokines associated with inflammatory reactions (IL-1β, IL-6, IL-8) were significantly upregulated, whereas genes encoding effector molecules, assisting the elimination of pathogens, C-reactive protein (CRP)-PII, hepcidin, lysozyme G1, lysozyme G2, C3 and IgDm, were significantly downregulated. The number of downregulated genes increased with the parasite burden. In spleen, 14 of 23 immune genes showed significant regulation and nine of these were upregulated, including genes encoding CRPI, CRPII, C3, hepcidin and transferrin. The general gene expression level was higher in spleen compared to liver, and although inflammation was induced in nematode-infected liver, the effector molecule genes were depressed, which suggests a worm-induced immune suppression locally in the liver.

One of the important issues in catfish farming is motile aeromonad septicaemia (MAS) disease caused by the bacterium Aeromonas hydrophila. This study aimed to find the MHC-II marker potential for marker-based selection to generate MAS disease resistance of African catfish. PCR method was applied to identify catfish (body length: 7-8 cm) population that have MHC-II marker. Fish with and without the marker were then challenged by intraperitonially injecting of 0.1 mL/fish with A. hydrophila (105 cfu/mL). The results showed that the survival of fish having MHC-II marker (77.50 ± 4.00%) was higher than that of fish without the marker (53.33 ± 4.77%). Fish carrying MHC-II marker fish has also higher total erythrocytes, total leukocytes, phagocytic activity, and hematocrit levels than that of fish without the marker. The PCR results using specific primer for MHC-II showed a specific DNA band of 426 bp in fish having the marker, while there were no DNA bands in fish without the marker. Results of the PCR analyses showed that the percentage of progenies carrying MHC-II marker was 80%, while progenies from broodstock without the marker was 0%; this indicated that MHC-II marker could be inherited to the offsprings. Thus, the MHC-II marker could be used as a molecular marker of MAS disease resistance catfish.