Protective efficacy of new-generation anticoccidial vaccine candidates against Eimeria infection in chickens: A meta-analysis of challenge trials.

Limitations of live oocyst anticoccidial vaccines in poultry have led to a search for the new generation of anticoccidial vaccines. Several sources may influence the protective efficacy of the new generation of anticoccidial vaccine candidates. Therefore, the objective of this study was to explore the sources influencing the protective efficacy (in terms of the lesion score and the oocyst output) of the new-generation anticoccidial vaccine candidates from the challenge trials in chickens, using meta-analysis techniques. The overall effect size was also estimated to get the overview of the protective efficacy. The study outcomes were the standardized mean difference (SMD) of the lesion score and the difference in mean (DM) of the oocyst output. Descriptive statistics of the oocyst decrease ratio (%) and anticoccidial index (ACI) were also presented. Relevant citations were retrieved from PubMed, Scopus, and Web of Science. Of 1524 retrieved citations, 63 were included for meta-analysis (60 for the lesion score and 44 for the oocyst output). Overall, the new generation of anticoccidial vaccine candidates partially protected chickens from coccidiosis because they significantly reduced the lesion score (SMD = -3.69, [95% CI: -4.08 to -3.29], P < 0.001) with high heterogeneity (I2 = 96.85%) and the oocyst output (DM = -1.48, [95% CI: -1.75 to -1.21], P < 0.001) with high heterogeneity (I2 = 99.69%). The median oocyst decrease ratio was 66.15% (a range from 4.27% to 95.93%, n = 125 subgroups). The median ACI was 164.71 (a range from 50.05 to 196.40, n = 115 subgroups). Vaccine platform and route of administration were identified as sources of heterogeneity for the lesion score and the oocyst output. However, severe publication bias threatened validity of the lesion score outcome. After accounting for other sources of variation, the anticoccidial vaccine candidates were shown to be less effective in reducing the oocyst output when the challenge dose, the length between the day of last immunization and the day of the challenge, or the length between the day of the challenge and the day of sampling, increased. In conclusion, although the new generation of anticoccidial vaccine candidates clearly showed a partial protection of chickens from coccidiosis in experimental trials, the protective efficacy was influenced by several sources, such as the vaccine platform and route of administration. Sources of high heterogeneity such as protein antigens are worth exploring when additionally relevant data are available. Therefore, additional experimental trials in chickens are required to better understand the protective efficacy of the new-generation anticoccidial vaccine candidates.

Differential induction of apoptosis by type A and B trichothecenes in Jurkat T-lymphocytes.

Several studies have shown that the mycotoxins T-2 toxin, diacetoxyscirpenol (DAS), deoxynivalenol (DON) and nivalenol (NIV) affect lymphocyte functioning. However, the molecular mechanisms underlying the immunomodulatory effects of these trichothecenes are not defined yet. In this study, the potency of the type A trichothecenes T-2 toxin and DAS, and the type B trichothecenes DON (and its metabolite de-epoxy-deoxynivalenol; DOM-1) and NIV to reduce mitochondrial activity and to induce apoptosis of Jurkat T cells (human T lymphocytes) were examined. T-2 toxin and DAS are much more cytotoxic at low concentrations than DON and NIV as shown by the AlamarBlue cytotoxicity assay. In addition, the mechanism whereby DON and NIV induced cytotoxicity is mainly via apoptosis as we observed phosphatidylserine externalization, mitochondrial release of cytochrome c, procaspase-3 degradation and Bcl-2 degradation. In contrast, type A trichothecenes reduce the mitochondrial activity at approximately 1000-fold lower concentrations than the type B trichothecenes, resulting in necrosis. These data suggest that the mechanisms resulting in cytotoxic effects are different for type A and type B trichothecenes.