Background: The independent and interactive effects of dietary fiber (DF) and threonine (Thr) were investigated in growing pigs challenged with either systemic E. coli lipopolysaccharide (LPS) or enteric Salmonella Typhimurium (ST) to characterise their effect on intestinal barrier function. Results: In experiment 1, intestinal barrier function was assessed via oral lactulose and mannitol (L:M) gavage and fecal mucin analysis in pigs challenged with E. coli LPS and fed low fiber (LF) or high fiber (HF) diets with graded dietary Thr. Urinary lactulose recovery and L:M ratio increased (P < 0.05) during the LPS inoculation period in LF fed pigs but not in HF fed pigs. Fecal mucin output was increased (P < 0.05) in pigs fed HF compared to LF fed pigs. In experiment 2, RT-qPCR, ileal morphology, digesta volatile fatty acid (VFA) content, and fecal mucin output were measured in Salmonella Typhimurium challenged pigs, fed LF or HF diets with standard or supplemented dietary Thr. Salmonella inoculation increased (P < 0.05) fecal mucin output compared to the unchallenged period. Supplemental Thr increased fecal mucin output in the HF-fed pigs (Fib × Thr; P < 0.05). Feeding HF increased (P < 0.05) VFA concentration in cecum and colon. No effect of either Thr or fiber on expression of gene markers was observed except a tendency (P = 0.06) for increased MUC2 expression with the HF diet. Feeding HF increased goblet cell numbers (P < 0.05).Conclusion: Dietary fiber appears to improve barrier function through increased mucin production capacity (i.e., goblet cell numbers, MUC2 gene expression) and secretion (i.e., fecal mucin output). The lack of effect of dietary Thr in Salmonella-challenged pigs provides further evidence that mucin secretion in the gut is conserved and, therefore, Thr may be limiting for growth under conditions of increased mucin production.

Pigs are capable of nitrogen salvage via urea recycling, which involves the movement of urea in the gastrointestinal tract. Aquaporins (AQP) and urea transporter B (UT-B) are involved in urea recycling in ruminants; however, their contribution to urea flux in the intestinal tract of the pig is not known. The objective of this study was to characterize the presence and relative contribution of known urea transporters to urea flux in the growing pig. Intestinal tissue samples (duodenum, jejunum, ileum, cecum, and colon) were obtained from nine barrows (50.8 ± 0.9 kg) and analyzed for mRNA abundance of UT-B and AQP-3, -7, and -10. Immediately after tissue collection, samples from the jejunum and cecum were placed in Ussing chambers for analysis of the serosal-to-mucosal urea flux ( Jsm-urea) with no inhibition or when incubated in the presence of phloretin to inhibit UT-B-mediated transport, NiCl2 to inhibit AQP-mediated transport, or both inhibitors. UT-B expression was greatest ( P < 0.05) in the cecum, whereas AQP-3, -7, and -10 expression was greatest ( P < 0.05) in the jejunum. The Jsm-urea was greater in the cecum than the jejunum (67.8 . 42.7 ± 5.01 µmol·cm−2·h−1; P < 0.05), confirming the capacity for urea recycling in the gut in pigs; however, flux rate was not influenced ( P > 0.05) by urea transporter inhibitors. The results of this study suggest that, although known urea transporters are expressed in the gastrointestinal tract of pigs, they may not play a significant functional role in transepithelial urea transport. NEW & NOTEWORTHY We characterized the location and contribution of known urea transporters to urea flux in the pig. Aquaporins are located throughout the intestinal tract, and urea transporter B is expressed only in the cecum. Urea flux occurred in both the jejunum and cecum. Transporter inhibitors had no affect on urea flux, suggesting that their contribution to urea transport in the intestinal tract is limited. Further work is required to determine which factors contribute to urea flux in swine.

The present study investigated the interactive effect of functional amino acid (AA) supplementation and dietary protein level on growth performance and immune status in Salmonella-challenged pigs. Thirty-two growing pigs (8 pigs/treatment; 13.9 ± 0.82 kg initial body weight) had ad libitum access to 1 of 4 experiment diets in a 2×2 factorial arrangement with factors of dietary protein (LP: Low, 16% protein vs. High: HP, 20% protein) and 2 levels of functional AA supply (AA-: basal vs. AA+: Thr, Met, and Trp provided at 20% above requirement). After 7 d of adaptation, pigs were orally inoculated with saline containing Salmonella typhimurium (ST). Performance parameters [average daily gain (ADG), feed intake, and gain:feed (GF)] were measured in the pre- and post-inoculation periods. Blood samples were collected on d0, 4 and 7 post-inoculation for serum haptoglobin and albumin analysis. Shedding of ST (d1, 2, 4 and 6 post-inoculation) and quantification in digesta (ileum, cecum and colon; d7 post-inoculation) were analyzed. There was no effect of diet on pre-inoculation performance (P &gt; 0.05). Pigs fed AA+ showed increased ADG (0.457 vs. 0.298 ± 0.051 kg/d; P &lt; 0.05) and a trend for improved GF (0.67 vs. 0.40 ± 0.07 kg/kg; P &lt; 0.10) post-inoculation compared to AA- regardless of dietary protein level. Feeding AA+ increased overall albumin levels (35.7 vs. 34.2 ± 0.9 g/L; P &lt; 0.05) and decreased overall haptoglobin levels (1.64 vs. 1.81 ± 0.12 g/L; P &lt; 0.05) and decreased overall shedding score of ST (2.27 vs. 2.51 ± 0.09; P &lt; 0.05) compared to AA-. The ST counts in cecal digesta increased (2.78 vs. 2.23 ± 0.18 Log10 cfu/g; P &lt; 0.05) in pigs fed HP compared to LP-fed pigs and ST counts in colon were reduced (2.08 ± 0.18 vs. 2.61 ± 0.19 Log10 cfu/g; P &lt; 0.05) in AA+ compared to AA- pigs. Supplementation of diets with specific functional AA improved performance and health status of pigs when exposed to an enteric disease challenge.