Three experiments were conducted to investigate the effects of beta-glucan supplementation on pig performance and immune function. In Exp. 1, 100 weaned pigs (8.65 +/- 0.42 kg of BW and 28 +/- 2 d of age) were used in a 35-d experiment to determine the effects of graded levels of beta-glucan. Pigs were randomly allotted to 1 of 5 treatments containing beta-glucan supplemented at 0, 25, 50, 100, or 200 ppm. Each treatment was replicated using 5 pens containing 4 pigs per pen. The ADG of pigs between d 14 to 28 and d 0 to 28 responded to dietary beta-glucan in a quadratic fashion (P < 0.05), whereas beta-glucan had no effect on ADFI and G:F in any period. In Exp. 2, 80 crossbred pigs (8.23 +/- 0.56 kg of BW and 28 +/- 2 d of age) were used in a 35-d experiment. Pigs were allotted to 1 of 2 dietary treatments (0 or 50 ppm of beta-glucan in the diet) using 10 pens with 4 pigs per pen. Pigs treated with beta-glucan had greater ADG in the 14- to 28-d (P = 0.05) and 0-to 28-d (P = 0.035) periods. The ADFI of pigs receiving beta-glucan was increased (P < 0.05) in the periods from 0 to 14, 0 to 28, and 28 to 35 d. The lymphocyte proliferation index in response to phytohemagglutinin (P = 0.051) and concanavalin A (P = 0.052) tended to decrease on d 14 in pigs supplemented with beta-glucan compared with pigs without supplementation. In Exp. 3, 24 barrows (8.89 +/- 0.20 kg of BW and 28 d of age) were used to investigate the immunological and somatotropic responses of pigs challenged with lipopolysaccharide (LPS). Experimental treatments were arranged in a 2 x 2 factorial, with the main effects of LPS challenge (saline vs. LPS) and dietary addition of beta-glucan (0 vs. 50 ppm). Pigs were raised individually in metabolic cages. Pigs were fed 0 or 50 ppm of beta-glucan for 28 d and then challenged with LPS (25 microg/kg of BW) or saline. After LPS injection, blood was obtained at 0, 1.5, 3, 4.5, 6, and 7.5 h to determine cytokine production and the somatotropic response. Dietary beta-glucan increased plasma interleukin-6 at 1.5, 3, and 4.5 h and tumor necrosis factor-alpha at 3 and 4.5 h and increased plasma interleukin-10 from 3 to 7.5 h after LPS challenge. The beta-glucan treatments had no effect on growth hormone. In conclusion, beta-glucan can selectively influence performance and partially offer benefits on somatotropic axis and immune function in weaned piglets challenged with LPS.

We investigated the anti-inflammatory role of conjugated linoleic acid (CLA) in inflammation-challenged weaned pigs and in in vitro cultured peripheral blood mononuclear cells (PBMCs). To test the hypothesis that inflammation responses can be attenuated by dietary CLA supplementation, we used an acute inflammation model in which pigs were injected with lipopolysaccharide (LPS). After 14 d of dietary supplementation with either 2% soybean oil or 2% CLA, half of the pigs in each diet group were challenged with LPS. Dietary CLA alleviated growth depression and prevented the elevations in production and mRNA expression of proinflammatory cytokines [i.e., interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha] induced by the LPS challenge. CLA enhanced the expression of interleukin-10 (IL-10) and peroxisome proliferator-activated receptor-gamma (PPARgamma) in spleen and thymus. To further elucidate the inhibitory effects and the mechanism of action of CLA on cytokine profiles (i.e., IL-1beta, IL-6, and TNF-alpha), PBMCs were isolated from weaned pigs and cultured in media containing cis-9, trans-11 (9c,11t) CLA and trans-10, cis-12 (10t,12c) CLA. Each CLA isomer suppressed the production and expression of IL-1beta, IL-6, and TNF-alpha, and enhanced PPARgamma activation and gene expression in cultured PBMCs. At the molecular level, the inhibitory actions of CLA on IL-1beta, IL-6, and TNF-alpha are attributable mainly to 10t,12c-CLA and the anti-inflammatory properties of CLA are mediated, at least in part, through a PPARgamma-dependent mechanism.

Twenty-four barrows were used to investigate the effects of beta-glucan on immune function in weaned piglets. Pigs (8.09 +/- 0.20 kg, 28 d of age) were fed a diet without or with supplemented beta-glucan (50 mg/kg feed). All pigs were injected with ovalbumin (OVA) on day 14 to investigate their humoral immune response. On day 28, lymphocytes were isolated from all pigs to determine the effects of beta-glucan on cellular immunity of pigs in vitro. Lymphocytes from six pigs of each group were incubated with 16 microg lipopolysaccharide (LPS) per ml culture medium, the remainder with an equivalent volume of culture medium alone. Samples were collected at 0, 3, 6, 12, 18, 24, and 48 h after LPS addition for determination of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and interleukin-10 (IL-10). On day 31, six pigs of each group were injected with either LPS (25 microg/kg BW) or an equivalent amount of sterile saline. Blood samples were collected at 3 h after LPS injection for analysis of IL-6, TNF-alpha, and IL-10 in plasma. The results indicated that dietary beta-glucan enhanced pig antibody response to OVA only in the first week after injection. In vitro, the increases of IL-6 and TNF-alpha in culture medium were partially dampened in pigs supplemented with beta-glucan when their lymphocytes were incubated with LPS, whereas the increase of IL-10 was potentiated. In vivo, dietary beta-glucan attenuated the increase of plasma IL-6 and TNF-alpha, and enhanced the increase of plasma IL-10 when pigs were challenged with LPS. These results demonstrate that beta-glucan can improve the humoral immunity of pigs and modulate cellular immunity of pigs by mitigating the elevation of pro-inflammatory cytokines and enhancing the increase of anti-inflammatory cytokines after an immunological challenge.

A total of 108 crossbred piglets (7.75 +/- 0.24 kg of BW) weaned at 28 d was used to study the interactive effects of beta-glucan obtained from the Chinese herb Astragalus membranaceus (AM) and Escherichia coli lipopolysaccharide (LPS) challenge on performance, immunological, adrenal, and somatotropic responses of weaned pigs. The treatments were in a 2 x 3 factorial arrangement; main effects were level of Astragalus membranaceus glucan (AMG; 0, 500, or 1,000 mg/kg; as-fed basis) and presence of immunological challenge (with or without LPS). The experiment included six replicate pens per treatment and three pigs per pen. Lipopolysaccharide challenges were conducted on d 7 and 21 of the trial. Blood samples were obtained from the vena cava from one pig per pen at 3 h after LPS challenge to determine plasma responses. Weight gain and feed:gain ratio were unaffected by glucan. However, there was a quadratic effect on feed intake (P < 0.05): pigs fed 500 mg of glucan/kg had the highest feed intake. Immunological challenge with LPS decreased weight gain (P = 0.02). An interaction (P = 0.01 to 0.09) between AMG and LPS was observed for glucose, IL-1beta, PGE2, and cortisol. Astragalus membranaceus glucan had a quadratic effect on the plasma concentrations of glucose, IL-1beta, PGE2, and cortisol (P < 0.05) after both LPS challenges. Plasma concentrations of glucose, IL-1beta, PGE2, and cortisol (P < 0.05) were all increased in LPS-challenged pigs compared with the control pigs after both LPS challenges. The IGF-I concentrations were less for LPS-challenged pigs than for unchallenged pigs. The lymphocyte proliferation response of peripheral blood induced by 5 microg of concanavalin A/mL (P < 0.01) and IL-2 bioactivity (P < 0.05) increased linearly with increasing addition of glucan. Pigs challenged with LPS had greater T-lymphocyte proliferation (P = 0.06) and IL-2 bioactivity (P = 0.07) than unchallenged pigs after the first immunological challenge but not after the second. In conclusion, although glucan did not improve pig performance under the conditions of the present experiment, when included at 500 mg/kg, it decreased the release of inflammatory cytokine and corticosteroid and improved the lymphocyte proliferation response of weanling piglets via enhanced IL-2 bioactivity.