Immune and anti-oxidant effects of in ovo selenium proteinate on post-hatch experimental avian necrotic enteritis

- In ovo selenium proteinate (BT) enhanced protection against avian necrotic enteritis.
- BT-treatment increased body weights and levels of serum antibodies against α-toxin and NetB toxin.
- BT-treatment decreased levels of serum MDA and affected serum CAT and SOD activities.
- BT-treatment increased intestinal levels of gene transcripts encoding IL-1β, IL-6, IL-8, and PRDX6.

This study was conducted to investigate the effects of in ovo administration of selenium (Se) incorporated into hydrolyzed soybean protein (B-Taxim [BT]) on protection against experimental avian necrotic enteritis (NE). Broiler eggs were injected with either 100 μl of PBS alone (BT0), or 20 or 40 μg/egg of BT in PBS (BT20, BT40) at 18 days of embryogenesis. On day 14 post-hatch, the chickens were uninfected or orally infected with 1.0 × 104 oocysts of Eimeria maxima (E. maxima). On day 18 post-hatch, E. maxima-infected chickens were orally infected with 1.0 × 109 CFU of Clostridium perfringens (C. perfringens). Compared with untreated and infected BT0 controls, BT20 and/or BT40 birds showed increased body weights, decreased fecal shedding of E. maxima oocysts, lower serum α-toxin and NetB levels, increased levels of serum antibodies against C. perfringens α-toxin and NetB toxin, decreased levels of serum malondialdehyde, reduced serum catalase and superoxide dismutase catalytic activities, and increased intestinal levels of gene transcripts encoding interleukin (IL)-1β, IL-6, IL-8, and peroxiredoxin-6, but decreased levels of transcripts for catalase and glutathione peroxidase. Interestingly, transcript levels for inducible nitric oxide synthase and paraoxonase/arylesterase 2 were decreased in the BT20 group and increased in the BT40 group, compared with BT0 controls. These results indicate that in ovo administration of broiler chickens with a Se-containing protein hydrolysate enhanced protection against experimental NE possibly by altering the expression of proinflammatory and anti-oxidant genes and their downstream pathways.