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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #424715

Research Project: Analysis of Genetic Factors that Increase Foodborne Pathogen Fitness, Virulence, and Antimicrobial Resistance Transfer, to Identify Interventions against Salmonella and Campylobacter in Food Animals

Location: Food Safety and Enteric Pathogens Research

Title: Host immunological responses in Ross 308 broilers fed anti-IL-10 diet during Eimeria maxima and Clostridium perfringens challenge

Author
item CARROLL, MICHAEL - Iowa State University
item FRIES-CRAFT, KRISTEN - Iowa State University
item CAO, YUYANG - Iowa State University
item Monson, Melissa
item SCHMITZ-ESSER, STEPHAN - Iowa State University
item BOBECK, ELIZABETH - Iowa State University

Submitted to: Poultry Science Association
Publication Type: Abstract Only
Publication Acceptance Date: 4/23/2025
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Understanding host response mechanisms to intestinal pathogen-induced tissue damage may lead to improved treatment methods for diseases such as necrotic enteritis, which reduces broiler performance and causes mortality. Three experimental replicates (R1, R2, R3) of Ross 308 broilers were placed in 32 cages (20 birds/cage) and received diets ' anti-IL-10 antibody, a dietary intervention to improve immune activation. R1 and R2 received 1x108 CFU Salmonella Typhimurium (ST) on day (d) 0. In a 2×3 factorial design, birds were then assigned to unchallenged control, Eimeria maxima (EM) challenge on d 14 (15,000 sporulated oocysts gavage), or EM d 14 + Clostridium perfringens d 18–19 (1×108 CFU) to induce necrotic enteritis (NE). Six birds per treatment were euthanized at baseline, peak infection, and post-infection. Intestinal tissue and digesta samples were collected to measure luminal IL-10 (ELISA) and visualize IL-10 and IFN' production via immunohistochemistry (IHC; HALO Area Quantification Module). ANOVA was completed in SAS 9.4 for host IHC and luminal content data (P < 0.05). RNA was purified from jejunal tissue (R3 only) at baseline and peak infection, sequenced on an Illumina NovaSeq 6000, and mapped to the chicken genome using STAR. DESeq2 identified differentially expressed genes (|log2 fold change| > 1; FDR = 0.05). In R1 and R2, baseline IL-10 was significantly greater in the duodenum of unchallenged vs. Salmonella-challenged (P < 0.05), and the anti-IL-10 diet had increased IL-10 vs. control (P = 0.006). Duodenum luminal IL-10 was higher at peak infection in birds challenged with NE vs. EM (P = 0.008). Birds fed the control diet in R3 had more IL-10 vs. birds fed anti-IL-10 in the duodenum at baseline and in the ceca post-infection (P < 0.05). NE increased IL-10 at peak infection in jejunum and ileum, while EM increased IL-10 in ceca post-infection (P < 0.05). Ileal IFN' production area trended towards an increase at peak NE challenge in R1 (P = 0.06), significantly differed in R2 at baseline (P = 0.03) and due to challenge (P = 0.02), and significantly increased due to challenge in R3 (P = 0.04). Jejunal transcriptomic contrasts for unchallenged vs. EM, unchallenged vs. NE, and EM vs. NE at peak infection showed 1,803, 1,353, and 0 significantly differentially expressed genes, respectively, with 56.6% shared between the first two contrasts. EM challenge upregulated genes involved in cell cycle, lipid metabolism, and B cell proliferation, while necrotic enteritis also increased defense response and catabolic metabolism genes. Overall, more differences in intestinal host responses, both cytokine production and transcriptional changes, were due to challenge type than diet.