This study was conducted to investigate the effects of a probiotic product incorporating Lactobacillus fermentum and Saccharomyces cerevisiae on the growth performance and intestinal immune status in broiler chickens. A total of six hundred ninety-six 1-d-old male Cobb broilers were randomly allotted by BW in 1 of 4 treatments for 6-wk trial. The dietary treatments included the basal diet (NC), and the basal diets supplemented with an antibiotic (100 mg of chlortetracycline/kg of diet; PC), 0.1%, or 0.2% probiotic product (containing 1 × 10(7) cfu/g of Lactobacillus fermentum JS and 2 × 10(6) cfu/g of Saccharomyces cerevisiae). Each treatment had 6 replicates with 29 broilers each. The ADG and feed efficiency were improved (P < 0.05) in broilers fed the probiotic diet compared with NC, and were similar to the PC group during 1 to 21 d. However, there were no significant differences in growth performance of broilers during 22 to 42 d among different dietary treatments. Chicks fed probiotics had higher proportions of CD3+, CD4+, and CD8+ T-lymphocytes, whereas the antibiotic diet decreased the proportion of CD8+ T-lymphocytes in the foregut of broilers at 21 and 42 d compared with the NC group. No significant difference was observed in the mRNA expression level of chicken B-cell marker chB6 (Bu-1) in the foregut of chickens among different treatments. Probiotic-supplemented diets increased (P < 0.05) the mRNA expression levels of Toll-like receptor (TLR) 2 and TLR 4 at 21 d, and only the TLR2 mRNA level at 42 d in the foregut of chickens, but did not change (P > 0.05) TLR7 mRNA expression compared with NC or PC. There was no significant difference in the above TLR mRNA levels in the intestine of broilers between PC and NC. These results indicated that the probiotic product incorporating Lactobacillus fermentum and Saccharomyces cerevisiae could stimulate intestinal T-cell immune system without decreasing growth performance in broilers during 1 to 21 d.

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This study examined the prebiotic effects of xylooligosaccharides (XOS) on intestinal characteristics, gut microbiota, cecal short-chain fatty acids, plasma calcium metabolism, and immune parameters of laying hens. A total of 1,080 White Lohmann laying hens (28 wk of age) was assigned to 6 dietary treatments that included XOS at concentrations of 0, 0.01, 0.02, 0.03, 0.04, or 0.05% for 8 weeks. Each treatment had 6 replicates with 10 cages (3 birds/cage). Blood, intestinal tissues, and cecal digesta samples were collected from chickens at the end of the experiment. Villus height, crypt depth, the villus to crypt (VH: CD) ratio, and the relative length of different intestinal sections were evaluated. Additionally, the number of microorganisms and the content of short-chain fatty acids in cecal digesta samples were determined. Plasma concentrations of immunoglobulin A (IgA), immunoglobulin G, immunoglobulin M (IgM), interleukin 2 (IL-2), tumor necrosis factor-α(TNF-α), 1, 25-dihydroxyvitamin D3 (1,25(OH)2D3), calcitonin (CT), and parathyroid hormone (PTH) were also determined. The results showed that villus height and the VH: CD ratio of the jejunum were increased (linear, P < 0.01) with the increase in dietary XOS concentration, and the relative length of the jejunum (P = 0.03) was increased significantly in XOS diets. Dietary supplementation of XOS significantly increased (linear, P < 0.01) the number of Bifidobacteria in the cecum; however, total bacteria count, Lactobacillus, and Escherichia coli in the cecum were not affected by XOS supplementation. In addition, inclusion of XOS increased (linear, P < 0.01) the content of butyrate in the cecum; and the content of acetic acid showed a linear increasing trend (P = 0.053) with increasing concentration of XOS in the diets. Supplementation with XOS increased (quadratic, P < 0.05) the content of 1,25(OH)2D3 in plasma. There were no significant differences (P > 0.05) in the content of CT and PTH among dietary treatments. Furthermore, dietary XOS increased contents of IgA (linear, P < 0.05), TNF-α (linear, P < 0.05), IgM (linear, P < 0.05; quadratic, P < 0.05), and IL-2 (quadratic, P < 0.05). Taken together, it was suggested that supplemental XOS can enhance the intestinal health and immune function of laying hens by positively influencing the intestinal characteristics, gut microbiota, cecal short-chain fatty acids, and immune parameters.

BackgroundRapid progression of residual tumor after radiofrequency ablation (RFA) of hepatocellular carcinoma has been observed increasingly. However, its underlying mechanisms remain to be clarified. The present study was designed to determine whether low temperature of RFA at the target sites facilitates rapid progression of residual hepatic VX2 carcinoma and to clarify the possible underlying mechanisms.MethodsThe residual VX2 hepatoma model in rabbits was established by using RFA at 55, 70 and 85°C. Rabbits that were implanted with VX2 hepatoma but did not receive RFA acted as a control group. The relationship between rapid progression of residual hepatic VX2 carcinoma and low temperature of RFA at the target sites was carefully evaluated. A number of potential contributing molecular factors, such as proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 9 (MMP-9), vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF) and Interleukin-6 (IL-6) were measured.ResultsThe focal tumor volume and lung metastases of RFA-treated rabbits increased significantly compared with the control group (P < 0.05), and the greatest changes were seen in the 55°C group (P < 0.05). Expression of PCNA, MMP-9, VEGF, HGF and IL-6 in tumor tissues increased significantly in the RFA-treated groups compared with the control group, and of the increases were greatest in the 55°C group (P < 0.05). These results were consistent with gross pathological observation. Tumor re-inoculation experiments confirmed that low temperature of RFA at the target sites facilitated rapid progression of residual hepatic VX2 carcinoma.ConclusionsInsufficient RFA that is caused by low temperature at the target sites could be an important cause of rapid progression of residual hepatic VX2 carcinoma. Residual hepatic VX2 carcinoma could facilitate its rapid progression through inducing overexpression of several molecular factors, such as PCNA, MMP-9, VEGF, HGF and IL-6.