This study evaluated whether arginine (Arg) supplementation could attenuate gut injury induced by Escherichia coli lipopolysaccharide (LPS) challenge through an anti-inflammatory role in weaned pigs. Pigs were allotted to four treatments including: (1) non-challenged control; (2) LPS-challenged control; (3) LPS þ 0·5 % Arg; (4) LPS þ 1·0 % Arg. On day 16, pigs were injected with LPS or sterile saline. At 6 h postinjection, pigs were killed for evaluation of small intestinal morphology and intestinal gene expression. Within 48 h of challenge, 0·5 % Arg alleviated the weight loss induced by LPS challenge (P¼ 0·025). In all three intestinal segments, 0·5 or 1·0 % Arg mitigated intestinal morphology impairment (e.g. lower villus height and higher crypt depth) induced by LPS challenge (P, 0·05), and alleviated the decrease of crypt cell proliferation and the increase of villus cell apoptosis after LPS challenge (P,0·01). The 0·5 % Arg prevented the elevation of jejunal IL-6 mRNA abundance (P¼ 0·082), and jejunal (P¼0·030) and ileal (P¼ 0·039) TNF-a mRNA abundance induced by LPS challenge. The 1·0 % Arg alleviated the elevation of jejunal IL-6 mRNA abundance (P¼ 0·053) and jejunal TNF-a mRNA abundance (P¼ 0·003) induced by LPS challenge. The 0·5 % Arg increased PPARg mRNA abundance in all three intestinal segments (P, 0·10), and 1·0 % Arg increased duodenal PPARg mRNA abundance (P¼ 0·094). These results indicate that Arg supplementation has beneficial effects in alleviating gut mucosal injury induced by LPS challenge. Additionally, it is possible that the protective effects of Arg on the intestine are associated with decreasing the expression of intestinal proinflammatory cytokines through activating PPARg expression.

Forty weaned barrows (5.32 +/- 0.3 kg BW) at 17 +/- 2 d of age were used to investigate the effects of feeding glutamine and spray-dried plasma on the growth performance, small intestinal morphology, and immune responses of Escherichia coli K88-challenged pigs. Pigs were allotted to four treatments including: 1) nonchallenged control (NONC); 2) challenged control (CHAC); 3) 7% (as-fed basis) spray-dried plasma (SDP); and 4) 2% (as-fed basis) glutamine (GLN). On d 11 after weaning, all pigs were fitted with an indwelling jugular catheter. On d 12 after weaning, pigs in the CHAC, SDP, and GLN groups were orally challenged with skim milk E. coli K88 culture, whereas pigs in the NONC group were orally inoculated with sterilized skim milk. Rectal temperatures and fecal diarrheic scores were recorded and blood samples collected at 0 (baseline), 6, 12, 24, 36, and 48 h after the challenge for serum hormone and cytokine measurements. At 48 h postchallenge, all pigs were killed for evaluation of small intestinal morphology. There was no effect of feeding SDP or GLN on growth performance during the 11-d prechallenge period (P = 0.13). At 48 h after the challenge, CHAC pigs had decreased ADG (P = 0.08) and G:F (P = 0.07) compared with the NONC pigs; however, SDP and NONC pigs did not differ in G:F, and GLN and NONC pigs did not differ for ADG and G:F. At 6, 36, and 48 h after the challenge, CHAC, SDP, and GLN pigs had increased rectal temperature relative to the baseline (P = 0.09). At 12 and 36 h after the challenge, CHAC pigs had the highest incidence of diarrhea among treatments (P = 0.08). Serum IL-6 and ACTH were not affected by treatment or time after E. coli challenge (P = 0.11). In proximal, midjejunum, and ileum, CHAC pigs had greater villous atrophy and intestinal morphology disruption than NONC pigs (P < 0.01), whereas SDP and GLN pigs had mitigated villous atrophy and intestinal morphology impairment after E. coli challenge. Pigs in the SDP had the lowest GH at 12 h and the greatest GH at 36 h after the challenge among treatments (P = 0.08). Pigs in the NONC had the highest IGF-1 at 12 and 36 h postchallenge (P < 0.04). These results indicate that feeding glutamine has beneficial effects in alleviating growth depression of E. coli K88-challenged pigs, mainly via maintaining intestinal morphology and function, and/or possibly via modulating the somatotrophic axis.

Seventy-two crossbred pigs (7.58 +/- 0.30 kg BW) weaned at 28 +/- 3 d of age were used to investigate the effects of fish oil supplementation on pig performance and on immunological, adrenal, and somatotropic responses following an Escherichia coli lipopolysaccharide (LPS) challenge in a 2 x 2 factorial design. The main factors consisted of diet (7% corn oil [CO] or 7% fish oil [FO]) and immunological challenge (LPS or saline). On d 14 and 21, pigs were injected intraperitoneally with either 200 microg/kg BW of LPS or an equivalent amount of sterile saline. Blood samples were collected 3 h after injection for analysis of interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), cortisol, growth hormone (GH), and insulin-like growth factor (IGF)-I. On d 2 after LPS challenge, peripheral blood lymphocyte proliferation (PBLP) was determined. Lipopolysaccharide challenge decreased ADG (487 vs. 586 g; P < 0.05) and ADFI (as-fed, 776 vs. 920 g; P < 0.05) from d 14 to 21 and ADG (587 vs. 652 g; P < 0.10) from d 21 to 28. Fish oil improved ADG (554 vs. 520 g; P < 0.10) and ADFI (891 vs. 805 g; P < 0.10) from d 14 to 21. On d 14, LPS challenge x diet interactions were observed for IL-1beta (P < 0.10), PGE2 (P < 0.001), and cortisol (P < 0.05) such that these measurements responded to the LPS challenge to a lesser extent (IL-1beta: 93 vs. 114 pg/mL, P < 0.05; PGE2: 536 vs. 1,285 pg/mL, P < 0.001; cortisol: 143 vs. 206 ng/mL, P < 0.05) in pigs receiving the FO diet than in pigs fed the CO diet. In contrast, among LPS-treated pigs, pigs fed the FO diet had higher IGF-I (155 vs. 101 ng/mL; P < 0.10) than those fed the CO diet. On d 21 among LPS-treated pigs, pigs fed FO had lower IL-1beta (70 vs. 84 pg/mL; P < 0.10) and cortisol (153 vs. 205 ng/mL; P < 0.05) than those fed CO. Pigs fed FO had lower PGE2 (331 vs. 444 pg/mL; P < 0.05) and higher IGF-I (202 vs. 171 ng/mL; P < 0.10) compared with those fed CO. Lipopolysaccharide challenge decreased GH (0.27 vs. 0.33 ng/mL; P < 0.05) on d 14, whereas it had no effect on GH on d 21. During both LPS challenge periods, the challenge increased PBLP when these cells were incubated with 8 (1.46 vs. 1.32; P < 0.10) or 16 microg/mL (1.46 vs. 1.30; P < 0.05) of concanavalin A. Fish oil had no effect on PBLP. These results suggest that FO alters the release of proinflammatory cytokines, which might lead to improved pig performance during an immunological challenge.

Seven hundred and twenty hatchling broilers were allotted to 12 treatment groups. Groups 1 and 2 were fasted for 48 h posthatch; groups 3 and 4 were fasted for 48 h followed by ad libitum access to a 1% glutamine (Gln) diet; groups 5 and 6 had ad libitum access to a common diet; groups 7 and 8 had access to a 1% Gln diet posthatch; groups 9 and 10 were fed regular Oasis hatchling supplement; and groups 11 and 12 were fed Oasis sprayed with 1% Gln for the first 48 h posthatch. The birds in treatment groups 2, 4, 6, 8, 10, 11, and 12 were vaccinated with Eimeria maxima posthatch, and all birds were orally challenged with high dose E. maxima on d 22. During the first 2 wk, birds in group 7 had the highest gain and feed efficiency among treatments (P < 0.01). Compared with birds in the nonGln groups, birds in the Gln group had higher gain, feed efficiency, and livability (P < 0.05). Among the Fast (groups 1 to 4), Feed (groups 5 to 8), and Oasis (groups 9 to 12) groups, birds in the Feed groups had the highest gain during d 0 to 21 (P < 0.01). During d 22 to 28, birds in the Fast groups had the lowest BW and livability (P < 0.01), and the nonvaccinated birds had lower gain and feed efficiency relative to vaccinated birds (P < 0.01). Birds in the Feed and Oasis groups had higher villus height (VH) of mid small intestine than Fast groups at d 2 and 7 (P < 0.05), and nonvaccinated birds had higher VH than vaccinated birds (P < 0.01) at d 7 after hatch. On d 14, there were differences in serum interferon-gamma (P < 0.05) levels among treatments. During d 22 to 28, vaccinated birds had lower lesion scores in the mid small intestine than nonvaccinated birds (P < 0.01), and birds in the Feed or Oasis groups had lower lesion scores compared with the Fast groups (P < 0.02). These results indicated the importance of immediate access to feed posthatch, the beneficial effects of feeding Oasis hatching supplement and Gln after hatch, as well as the necessity of the vaccination program against coccidiosis challenge.

Two experiments were conducted to compare the effects of feeding organic acids and antibiotic growth promoters in weaned pigs. In Exp. 1, 96 nursery pigs (Large White×Landrace; initial weight 7.80±0.07 kg) were randomly allotted into one of four dietary treatments. Pigs in treatment 1 were fed a complex starter diet. Treatments 2 to 4 were the same as treatment 1 but supplemented with antibiotics (200 ppm chlortetracycline plus 60 ppm Lincospectin), 0.5% potassium diformate or 0.5% dry organic acid blend ACTIVATE Starter DA (ASD). During the 4-week post-weaning period, pigs fed ASD or antibiotics had better gain (p = 0.03) and feed efficiency (p = 0.04) than pigs fed the control diet. On d 14 post-weaning, pigs fed the control diet had the lowest fecal lactobacilli count among all dietary treatments (p = 0.02), whereas pigs fed ASD or antibiotics had a trend for lower fecal E. coli count compared to the control pigs (p = 0.08). Serum insulin-like growth factor-1 (IGF-1) of pigs fed ASD did not differ from pigs fed the control diet (p>0.05) at d 14 after weaning. In Exp. 2, 24 weaned pigs (Large White×Long White; initial weight 5.94±0.33 kg) were allotted into four groups and housed individually. Pigs were fed a control diet or diets supplemented with antibiotics (100 ppm colistin sulfate, 50 ppm Kitasamycin plus 60 ppm Olaquindox), 0.5% or 1% ASD. All pigs were orally challenged with E. coli K88 + on d 5. During d 5 to 14 after challenge, pigs fed antibiotics, 0.5% or 1% ASD had better gain (p = 0.01) and feed efficiency (p = 0.03) than pigs fed the control diet. On d 14, compared to the control pigs, pigs fed 0.5% ASD had higher lactobacilli in the duodenum and pigs fed 1% ASD and antibiotics had a trend for higher lactobacilli in the ileum (p = 0.08). Pigs fed antibiotics, 0.5% or 1% ASD diets tended to have decreased ileal E. coli count compared to those fed the control diet (p = 0.08). Serum interleukin-6 and cortisol and digesta pH values were not affected by treatment or time. These results indicate that feeding ASD can improve the growth performance of weaning pigs, mainly via modulating intestinal microflora populations without affecting gastrointestinal pH or immune indices.