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

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-1ß, 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-1ß 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.

Regular swimming exercise prevented the acute and persistent mechanical muscle hyperalgesia by modulation of macrophages phenotypes and inflammatory cytokines via PPARγ receptors.

Physically active individuals are less likely to develop chronic pain, and physical exercise is an established strategy to control inflammatory diseases. Here, we hypothesized that 1) peripheral pro-inflammatory macrophages phenotype contribute to predisposition of the musculoskeletal to chronic pain, and that 2) activation of PPARγ receptors, modulation of macrophage phenotypes and cytokines through physical exercise would prevent persistent muscle pain. We tested these hypotheses using swimming exercise, pharmacological and immunochemical techniques in a rodent model of persistent muscle hyperalgesia. Swimming prevented the persistent mechanical muscle hyperalgesia most likely through activation of PPARγ receptors, as well as activation of PPARγ receptors by 15d-PGJ2 and depletion of muscle macrophages in sedentary animals. Acute and persistent muscle hyperalgesia were characterized by an increase in pro-inflammatory macrophages phenotype, and swimming and the 15d-PGJ2 prevented this increase and increased anti-inflammatory macrophages phenotype. Finally, IL-1ß concentration in muscle increased in the acute phase, which was also prevented by PPARγ receptors activation through swimming. Besides, swimming increased muscle concentration of IL-10 in both acute and chronic phases, but only in the persistent phase through PPARγ receptors. Our findings suggest physical exercise activates PPARγ receptors and increases anti-inflammatory responses in the muscle tissue by modulating macrophages phenotypes and cytokines, thereby preventing the establishment of persistent muscle hyperalgesia. These results further highlight the potential of physical exercise to prevent chronic muscle pain.

Taenia hydatigena larvae vesicular concentrate reduces the egg shedding of Haemonchus contortus associated with the overexpression of abomasal cytokines in lambs.

The expression patterns of some cytokines were compared by RT-qPCR between lambs with and without Taenia hydatigena larvae vesicular concentrate (ThLVC) administration and subsequent infection with Haemonchus contortus. Lambs that received ThLVC prior to infection with H. contortus showed lower (p < 0.03) cumulative FEC (AUC = 18450 ± 3384) than infected lambs who did not receive ThLVC (AUC = 31081 ± 3277). Lambs infected with H. contortus, in general, overexpressed Th1 and Th2 cytokines in abomasal mucosa and abomasal lymph nodes, which seems to indicate a generalized and nonpolarized activation of the immune response by H. contortus. The main immunomodulatory effects of ThLVC were observed in the abomasal fundic region. The lambs that were given ThLVC prior to infection strongly overexpressed most of the studied cytokines representing the Th1 (IFNγ and IL2) and Th2 profiles (IL4, IL5, IL6 and IL10), proinflammatory cytokines (SOD1 and PRDX6) and IgE receptor; in contrast, lambs that were infected but did not receive ThLVC only moderately overexpressed IFNγ, IL4 and IL6. The absence of the significant overexpression of cytokines in lambs that only received ThLVC suggests that this derived from T. hydatigena does not have a stimulating effect per se; however, the presence of H. contortus did produce the highest expression (p < 0.01) cytokine profile among lambs that received ThLVC prior to infection compared to those who did not receive it, so its effect seems to be immunomodulatory and not only immunostimulatory.

Anterior chamber associated immune deviation to cytosolic neural antigens avoids self-reactivity after optic nerve injury and polarizes the retinal environment to an anti-inflammatory profile.

It has been hypothesized that anterior chamber-associated immune deviation (ACAID) to neural antigens induced prior to central nervous system injury can inhibit self-reactivity and lessen secondary degeneration. This work evaluated the effect of ACAID induced to three neural tissue-derived extracts (whole extract, cytosolic extract, CE; or organelle-membrane extract) prior to optic nerve injury on retinal ganglion cell (RGC) survival. The results show that only ACAID to the CE increased RGC survival at 7 and14 days post-injury (dpi). This effect was achieved by retinal polarization towards an anti-inflammatory profile, driven by regulatory T cells and M2-type macrophages at 7 dpi.