A 2 £ 2 factorial experiment was conducted to investigate the interactions between laminarin (LAM; 0 and 300 parts per million (ppm)) and fucoidan (FUC; 0 and 240 ppm) levels on intestinal morphology, selected microbiota and inflammatory cytokine gene expression in the weaned pig. There was an interaction between LAM and FUC supplementation on the Enterobacteriaceae population (P,0·05) and the abundance of attaching and effacing Escherichia coli (AEEC) strains (P, 0·05) in the colon. Pigs offered the FUC diet had a reduced Enterobacteriaceae population compared with pigs offered the basal diet. However, the effect of FUC on the Enterobacteriaceae population was not observed when combined with LAM. Pigs offered the LAM diet had reduced abundance of AEEC strains compared with pigs offered the basal diet. However, there was no effect of LAM on the abundance of AEEC strains when combined with FUC. There was an interaction between LAM and FUC supplementation on villous height (P,0·01) and the villous height:crypt depth ratio (P,0·01) in the duodenum. Pigs offered the LAM or FUC diet had an increased villous height and villous height:crypt depth ratio compared with pigs offered the basal diet. However, there was no effect of the LAM and FUC combination diet on intestinal morphology. Pigs offered the LAM-supplemented diets had a lower IL-6 (P, 0·05), IL-17A (P, 0·01) and IL-1b (P,0·01) mRNA expression in the colon compared with pigs offered the diets without LAM. In conclusion, supplementation with either LAM or FUC alone modified intestinal morphology and selected intestinal microbiota, but these effects were lost when offered in combination.

In the present study, two experiments were conducted to (1) evaluate the effect of laminarin and/or fucoidan on ileal morphology, nutrient transporter gene expression and coefficient of total tract apparent digestibility (CTTAD) of nutrients and (2) determine whether laminarin inclusion could be used as an alternative to ZnO supplementation in weaned pig diets. Expt 1 was designed as a 2 £ 2 factorial arrangement, comprising four dietary treatments (n 7 replicates, weaning age 24 d, live weight 6·9 kg). The dietary treatments were as follows: (1) basal diet; (2) basal diet þ 300 ppm laminarin; (3) basal diet þ 240 ppm fucoidan; (4) basal diet þ 300 ppm laminarin and 240 ppm fucoidan. There was an interaction between laminarin and fucoidan on the CTTAD of gross energy (GE) (P,0·05) and the expression of sodium -glucose-linked transporter 1 (SGLT1/SLC5A1) and GLUT1/SLC2A1 and GLUT2/SLC2A2 (P,0·05) in the ileum. The laminarin diet increased the CTTAD of GE and increased the expression of SGLT1, GLUT1 and GLUT2 compared with the basal diet. However, there was no effect of laminarin supplementation on these variables when combined with fucoidan. Expt 2 was designed as a complete randomised design (n 8 replicates/ treatment, weaning age 24 d, live weight 7·0 kg), and the treatments were (1) basal diet, (2) basal diet and laminarin (300 ppm), and (3) basal diet and ZnO (3100 ppm, 0-14 d, and 2600 ppm, 15-32 d post-weaning). The laminarin diet increased average daily gain and gain: feed ratio compared with the basal diet during days 0 -32 post-weaning (P,0·01) and had an effect similar to the ZnO diet. These results demonstrate that laminarin provides a dietary means to improve gut health and growth performance post-weaning.

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The algal polysaccharides laminarin (LAM) and fucoidan (FUC) have potent anti-inflammatory activities in the gastrointestinal tract. Our objective was to examine the impact of prior consumption of LAM and/or FUC on pathology and inflammation following a dextran sodium sulfate (DSS) challenge in pigs. Pigs (n 7/group) were assigned to one of five experimental groups for 56 d. From 49–55 d, distilled water or DSS was administered intragastrically. The experimental groups were: (1) basal diet + distilled water (control); (2) basal diet + DSS (DSS); (3) basal diet + FUC + DSS (FUC + DSS); (4) basal diet + LAM + DSS (LAM + DSS); and (5) basal diet + LAM + FUC + DSS (LAMFUC + DSS). The DSS group had decreased body-weight gain (P < 0·05) and serum xylose (P < 0·05), and increased proximal colon pathology score (P < 0·05), diarrhoeal score (P < 0·001) and colonic Enterobacteriaceae (P < 0·05) relative to the control group. The FUC + DSS (P < 0·01), LAM + DSS (P < 0·05) and LAMFUC + DSS (P < 0·05) groups had improved diarrhoeal score, and the LAMFUC + DSS (P < 0·05) group had improved body weight relative to the DSS group. The FUC + DSS group (P < 0·001), LAM + DSS group (P < 0·05) and LAMFUC + DSS group (P < 0·001) had lower IL-6 mRNA abundance relative to the DSS group. The LAM + DSS group had reduced Enterobacteriaceae in proximal colon digesta relative to the DSS group (P < 0·05). In conclusion, FUC or a combination of FUC and LAM improved body-weight loss, diarrhoeal scores and clinical variables associated with a DSS challenge in pigs, in tandem with a reduction in colonic IL-6 mRNA abundance.

In the present study, a 2 £ 2 factorial arrangement was conducted to investigate the effect of maternal supplementation with seaweed extracts (2 SWE v. þSWE, n 20) from day 83 of gestation until weaning (day 28) on post-weaning (PW) growth performance, faecal score, faecal enterotoxigenic Escherichia coli (ETEC) toxin quantification, intestinal histology and cytokine mRNA of unchallenged and ETEC-challenged pigs. Pigs were ETEC challenged on day 9 PW. There was a maternal treatment £ challenge (SWE £ ETEC) interaction effect on growth performance and faecal score (P,0·05). Pigs from SWE-supplemented sows and ETEC-challenged (SE) had higher average daily gain (ADG) during 0 -13 d PW and reduced faecal score during 0 -72 h post-challenge than those from basal-fed sows and ETEC-challenged (BE) (P,0·05). However, there was no difference between unchallenged pigs from the SWE-supplemented sows (SC) and basal-fed sows (BC) (P.0·10). Pigs from the SWE-supplemented sows had reduced heat-labile enterotoxin gene copy numbers than those from the basal-fed sows (P,0·05). Maternal SWE supplementation increased the villus height in the ileum of pigs (P,0·05). There was a SWE £ ETEC interaction effect (P,0·05) on IL-6 mRNA and a SWE £ gastrointestinal (GI) region interaction effect (P,0·05) on transforming growth factor-b1 (TGF-b1) and TNF-a mRNA. IL-6 mRNA was down-regulated in SC pigs than BC pigs (P,0·05). However, there was no difference in IL-6 mRNA between SE and BE pigs. The mRNA of TGF-b1 and TNF-a was down-regulated in the colon of pigs from the SWE-supplemented sows compared with those from the basal-fed sows (P, 0·05). However, there was no difference in TGF-b1 and TNF-a mRNA in the ileum between the pigs from the SWE-supplemented sows and basal-fed sows. In conclusion, maternal SWE supplementation improves ADG and the aspects of GI health of weaned pigs following an ETEC challenge.Key words: Enterotoxigenic Escherichia coli K88 challenge: Inflammatory cytokines: Pig performance: Seaweed extracts Enterotoxigenic Escherichia coli (ETEC) K88 is a major cause of diarrhoea in neonates and recently in weaned pigs (1,2) . It results in reduced growth rate, increased morbidity and mortality, and great economic loss in pig production worldwide (3,4) . Post-weaning (PW) diarrhoea due to ETEC K88 generally occurs in pigs 3-10 d PW (5,6) . ETEC K88 colonises in the small intestine and releases specific enterotoxins that impair intestinal barrier function, which indirectly induces fluid losses (4 -6) . Several factors, such as stress of weaning, lack of milk and dietary changes, contribute to the severity of the disease. Furthermore, weaning is often associated with undesirable morphological and physiological changes in the gastrointestinal (GI) tract that is related to a reduced voluntary feed intake and, subsequently, susceptibility to intestinal health imbalance (7,8) . The ban on the inclusion of antibiotic growth promoters in weaning pig diets in Europe (European Community Regulation no. 1831/2003) has been associ...