Host immunological response of Ross 308 broilers fed an anti-IL-10 antibody to Eimeria and Clostridium perfringens challenge.
Understanding host response mechanisms may lead to improved management of poultry diseases such as necrotic enteritis. Ross 308 broilers (20 birds/cage, 32 cages) received diets ± anti-interleukin-10 (IL-10) antibody, an intervention to improve immune activation, in three experimental replicates (R1, R2, R3). R1 and R2 received 1 × 108 colony forming units (CFU) Salmonella Typhimurium on day (d) 1. On d 14, birds were assigned to unchallenged control or 15,000 sporulated Eimeria maxima oocyst gavage challenge, with a subset receiving E. maxima + Clostridium perfringens (1 × 10⁸ CFU d 18-19) to induce necrotic enteritis. Intestinal tissue and digesta samples were collected from 6 birds/treatment at baseline (d 14), peak infection (d 21), and post-peak infection (d 25) to measure luminal IL-10 (ELISA), interferon gamma (IFNγ) via immunohistochemistry, and IL-10, CD4, CD8, CD25, and KUL01 via RNAscope. Data were analyzed via two-way ANOVA (P ≤ 0.05). In R3, baseline duodenal IL-10 was 458 ng/mg protein greater in birds fed the control diet, while E. maxima + C. perfringens inoculation increased jejunal and ileal IL-10 content by 528 and 649 ng/mg protein at peak infection (P < 0.05). In R2, peak jejunal tissue % IL-10 area increased during E. maxima + C. perfringens challenge (P < 0.05). Baseline and peak jejunal R3 RNA was sequenced on an Illumina NovaSeq 6000, mapped to the chicken genome, and differential expression identified with DESeq2 (|log₂ fold change| > 1; FDR ≤ 0.05). At peak, E. maxima challenge overrepresented genes involved in cell cycle, lipid metabolism, and B cell proliferation (P < 0.002), while E. maxima + C. perfringens overrepresented defense response and catabolic process terms (P < 0.0001). Sex altered the host immune response to challenge (P < 0.05), while E. maxima ± C. perfringens induced a similar host immune response regardless of dietary anti-IL-10. Overall, pathogenic challenge status was the primary driver of host immune response with the effect of anti-IL-10 antibody influenced by S. Typhimurium.