Modulation of expression of proinflammatory genes and humoral immune response following immunization or infection with Aeromonas hydrophila in silver catfish (Rhamdia quelen).

银鲶(Rhamdia quelen)接种嗜水气单胞菌或感染后促炎基因表达和体液免疫反应的调节

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作者:Soveral Lucas de Figueiredo, de Almeida Paola Aparecida, Kreutz Yasmin, Ribeiro Vitoria Agnoletto, Frandoloso Rafael, Kreutz Luiz Carlos
The early immune-related events arising from the interaction of antigen and innate immune cells are central to modulating the acquired immune response. Ideally, the immunizing antigen should elicit immunological changes similar to that observed after infection with the wild type pathogen. Here, we evaluated early changes on the expression of selected proinflammatory genes (TNF-α, IL-1β, IRAK4 and myeloperoxidase) and innate immune parameters (serum myeloperoxidase, lysozyme and complement hemolytic activity) in silver catfish vaccinated or infected with Aeromonas hydrophila, the etiological agent of hemorrhagic septicemia. The humoral immune response and resistance to challenge were also evaluated in vaccinated and placebo inoculated fish. We found that the expression of TNF-α and IL-1β genes was higher (p<0.05) in vaccinated or infected fish at 24 h post inoculation (p.i) compared to the control group but returned to basal levels at 72 h p.i. The expression of IRAK4 gene, however, was not altered by vaccination or infection. In addition, the natural hemolytic activity of complement was higher (p<0.05) at 24 h and 72 h p.i. in the vaccinated and infected groups; serum myeloperoxidase was higher (p<0.05) in these groups but only at 24 h p.i. and lysozyme activity was higher (p<0.05) only in the infected group at 72 h p.i. Furthermore, vaccination induced the production of IgM-like antibodies and protection to challenge with the A. hydrophila. Our results indicate that the vaccine formulation induces an immune response similar to that induced by the infecting pathogen and might be a valuable tool in the prophylaxis of hemorrhagic septicemia in silver catfish.

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