Stress-associated β -glucan administration stimulates the TLR - MYD88 - NFKB1 signaling pathway in Nile tilapia (Oreochromis niloticus).

There is evidence that the administration of β-glucan can effectively activate several defense mechanisms, such as the Tlr-Myd88-Nfkb1 pathway that induces the expression of immune cytokines. Thus, the objective of this work was to evaluate whether β-glucan acts on the mechanisms of gene transcription via the Tlr-Myd88-Nfkb1 pathway in Nile tilapia under stress after challenge with Streptococcus agalactiae. Therefore, we evaluated the expression of immune system genes such as toll-like receptors 1 (tlr1), toll-like receptors 2 (tlr2), primary myeloid differentiation response gene (myd88) and nuclear factor kappa B1 (nfkb1).

β-glucan mimics tissue damage signaling and generates a trade-off between head kidney and spleen to activate acquired immunity in vaccinated tilapia (Oreochromis niloticus).

The association of vaccines with immunostimulants such as β-glucan, promote the production of cytokines, competent immune cells and antibodies. However, differences between β-glucan types and trials make it difficult to understand β-glucan's mechanism of action. In this study, three trials were carried out with control and fish fed β-glucan, the first trial occurred at 15 days; the second trial occurred at 30 days when we associated β-glucan and vaccine; and the third trial occurred at 15 days post-challenge with Streptococcus agalactiae in tilapia (O.