Fermentable
carbohydrates may enhance the ability of the gastrointestinal tract to defend against pathogenic
infection. We hypothesized that a
mannose-rich,
galactoglucomannan oligosaccharide-
arabinoxylan (GGMO-AX) complex would positively impact immune status and prevent
weight loss resulting from acute
coccidiosis (Eimeria acervulina)
infection of chicks. Using a completely randomized design, 1-d-old commercial broiler chicks (n = 160; 4 replications/treatment; 5 chicks/replication) were assigned to one of 4 corn-soybean meal-based diets containing supplemental GGMO-AX (0, 1, 2, or 4%) that replaced dietary
cellulose. On d 9 posthatch, an equal number of chicks on each diet were inoculated with either distilled water (
sham control) or E. acervulina (1 × 10(6) oocysts). All birds were euthanized on d 7 postinoculation (PI) for collection of cecal contents and duodenal tissue. Overall, BW gain of chicks was not affected by diet PI, whereas
infection decreased (P < 0.01)
weight gain on d 0 to 7 PI. Feed intake was not affected by dietary treatment, but
infection decreased (P < 0.01) feed intake on d 0 to 7 PI. Overall,
infection, but not diet, decreased (P < 0.01) G:F on d 0 to 7 PI. Cecal
propionate concentrations were independently affected by
infection and diet, while
butyrate concentrations were affected only by
infection (P = 0.02). Cecal Bifidobacterium spp. populations were affected (P < 0.01) by diet, with the 2% GGMO-AX resulting in the highest cfu/g of cecal contents (on a DM basis).
Messenger RNA expression of all duodenal
cytokines evaluated was affected by
infection status (P ≤ 0.02) but not by dietary treatment alone. Supplementing 4% GGMO-AX consistently resulted in the greatest fold change in proinflammatory
cytokine expression, while inhibiting antiinflammatory
cytokine expression, which indicates a more robust innate immune response. Despite decreasing performance, 4% dietary GGMO-AX improved select fermentation indices and the innate intestinal immune response to an acute E. acervulina
infection.