132 The impact of F18 ETEC challenge on intestinal integrity and immune response of nursery pigs and the potential protective effects of direct-fed microbial blends

摘要

The objectives were to investigate the impact of an F18 ETEC challenge on localized immune responses and intestinal function of piglets, and to evaluate potential protective effects of direct-fed microbial blends (DFM1 and DFM2). Thirty-six pens of 3-wk old weaned piglets (2 pigs/pen; BW=6.42 ± 0.22 kg; L337 X Camborough, PIC, Hendersonville, TN) were assigned to one of four treatments: 1) NC: Non-challenged (n = 10), 2) PC:F18 ETEC challenged (n = 10), 3) PC+DFM1 (n = 8) or 4) PC+DFM2 (n = 8). Pigs were either sham-infected with saline or orally challenged with ETEC on d 7 (d 0 post-inoculation, dpi). On dpi 10, ileal mucosa was collected for disaccharidase quantification and whole ileal tissue was collected for immune marker and tight junction protein analysis via qRT-PCR. Data were analyzed using PROC MIXED of SAS (9.4) with dietary treatment as a fixed effect and pen as the experimental unit. There were no differences in lactase activity (P > 0.10). Sucrase and maltase activity increased in PC vs. NC (P < 0.05). Ileal mRNA abundance of zonula occludens-1 (ZO-1) decreased in PC and DFM1 compared with NC (P < 0.05). DFM2 increased ZO-1 compared with PC (P < 0.05). There was no difference in claudin-1 mRNA (P > 0.10). Cluster of differentiation 14 (CD14) mRNA was elevated in challenged pigs compared with NC (P < 0.05). Interleukin-10 (IL-10) tended to be elevated in both DFM treatments compared with PC (P < 0.10). All challenged treatments tended to have elevated tumor necrosis factor-a (TNFa) abundance vs. NC (P < 0.10). There were no differences in IL-1b, IL-6, or toll-like receptor 4 (TLR4) mRNA abundance (P > 0.10). In conclusion, the ETEC challenge increased CD14, tended to increase TNFa, and decreased ZO-1 mRNA abundance, indicating activation of intestinal inflammation and impaired intestinal barrier integrity. DFM2 may improve intestinal barrier integrity impaired by ETEC as evidenced by increased ZO-1 mRNA.