Direct-fed microbials (DFM) could serve as a potential alternative to the feeding of antibiotics in poultry production. In this study, the effects of providing a DFM were compared with the feeding of salinomycin on intestinal histomorphometrics, and microarchitecture was examined. Broiler chicks (n=18 per treatment; trials 1 and 2) were fed a standard starter diet (control), control+PrimaLac (DFM; 0.3% wt/wt), and control+salinomycin (SAL; 50 ppm) from hatch to 21d. The birds were euthanized on d 21, and the ileal, jejunal, cecal, and colon tissues were dissected. Samples were examined by light microscopy (jejunum and ileum; trial 1) and scanning electron microscopy (ileum, cecum, and colon; trial 2). Feeding of the DFM increased intestinal muscle thickness (P<0.05) up to 33% compared with the control treatment. The DFM group also had increased villus height and perimeter (P=0.009 and 0.003, respectively) in jejunum. Segmented filamentous-like bacteria were less numerous in DFM-treated chicks than in the control chicks. Very few segmented filamentous-like bacteria were found near other microbes in the ileum. The DFM chicks had a larger number of bacteria positioned over or near goblet cells and in intervilli spaces. Bacteria in the colon were observed to be attached primarily around and within the crypts. Mucous thickness was less, and the density of bacteria embedded in the mucous blanket appeared to be lower in DFM-treated animals than in the control in all intestinal segments. The birds fed SAL had fewer bacteria and enterocytes in the ileum than in the control-and DFM-treated birds, and they had thicker and fewer microvilli. Because gastrointestinal track colonization by the DFM organisms can prevent the attachment of pathogens to the epithelium, spatial relationships, in this study, demonstrate the functionality of DFM and probiotics in preventing disease. It also supports previous observations that the feeding of salinomycin may alter intestinal function.
Two lines of turkey poults, one selected for rapid growth at 16 wk of age (F line) and the other a randombred control line (RBC2) were used to investigate the effect of selection for rapid growth on jejunal O2 consumption and glucose transport as well as whole-body O2 consumption. All trials used unsexed poults and were designed as a randomized complete block with day and line as independent variables. In Trial 1, 120 turkey poults, fed a standard starter ration (25.5% CP), were used to examine the effect of selection on feed intake, body weight gain, and efficiency from hatching (Day 0) to 13 d of age. At Day 14, 36 of 60 birds from each line were killed to measure intestinal length and weight and jejunal O2 consumption after 18 h of feed deprivation. Compared with the RBC2 line, the F line had relatively shorter but heavier small intestinal segments when adjusted by 18 h feed-deprived body weight (FBW; P < 0.001). The F line consumed more O2 over the entire jejunum adjusted to FBW than RBC2 line (43.8 vs 34.6 nmol O2/min.g FBW; P < 0.001). Jejunal ouabain- and cycloheximide-sensitive O2 consumption were greater (P < 0.05) in the F line. In Trial 2, 16 14-d-old poults from each line were used to measure in vitro jejunal glucose transport rate. There was no difference in glucose transport of the jejunum (nanomoles per minute per gram of FBW) between the lines. In Trial 3, 20 poults from each line were used to measure whole-body O2 consumption at 7 to 10 d of age. The F and RBC2 lines had similar whole-body O2 consumption rate per gram of FBW. These data suggest that selection of turkeys for rapid growth at 16 wk of age did not increase efficiency of jejunal glucose uptake in 14-d-old turkey poults.
The current study investigated whole-body O2 consumption, intestinal O2 consumption, and intestinal inflammation status through mucosal cytokine production on broiler chicks fed the direct-fed microbial PrimaLac. One hundred twenty 1-d-old broiler chicks were randomly assigned to 1 of 3 experimental diets: standard starter diet (control), standard starter diet with added salinomycin (SAL), and standard starter diet with added PrimaLac (DFM). Birds were housed in 2 separate rooms, the control and SAL treatments in one room and the DFM in another. Intact ileal and cecal samples were collected on d 19, 20, and 21 after measuring whole-body O2 consumption using indirect calorimetry. The O2 up-take of ileal tissue was measured using an in vitro O2 monitor. Analysis of intestinal immune status of broilers was measured by the relative differences in mRNA of both pro- and antiinflammatory cytokines: interleukin-(IL) 1beta, IL-6, and IL-10 using real-time reverse transcription-PCR. Broilers exhibited a 6 to 16% decrease in whole-body energy expenditures and up to a 47% decrease (P<0.05) in ileal energy expenditures in the DFM group compared with other treatments. The reverse transcription-PCR data demonstrated that DFM consortium numerically altered both pro- and antiinflammatory cytokines within the ileum of 19-d posthatch broilers. These data suggest that direct-fed microbials like PrimaLac increase metabolic efficiency via changes in intestinal physiology and metabolism.
The effects of epidermal growth factor on intestinal glucose transport were examined in mice. Glucose transport measurements were performed using an in vitro assay system that estimated the rate of accumulation of [3H]3-O-methyl-D-glucose. In Experiment 1, two-mo-old male and female mice were subcutaneously injected once daily with 0, 150 or 300 micrograms epidermal growth factor/kg body weight for 3 d. Jejunal glucose active transport was increased in a dose-dependent manner. There were no gender-related differences in intestinal glucose transport or the response to exogenous epidermal growth factor. In Experiment 2, 2-, 10- and 18-mo-old mice were administered 0 or 300 micrograms epidermal growth factor/kg body weight using a treatment similar to that used in Experiment 1. Active intestinal glucose transport was 30% greater in response to epidermal growth factor in each of the three age groups. Ouabain-sensitive and -insensitive jejunal oxygen consumption was increased in response to epidermal growth factor such that total jejunal respiration was stimulated 15 to 31%. The epidermal growth factor related percentage increase in glucose absorption was similar to the percentage increase in oxygen consumption such that the apparent energetic efficiency of glucose transport was unaffected. In both experiments, the active component of glucose transport was increased by epidermal growth factor while passive transport was not affected. Jejunal morphology and mucosal DNA and protein concentration were not altered by epidermal growth factor treatment. Epidermal growth factor-induced increases in intestinal absorption was not attributable to mucosal hyperplasia.
The effects of in vitro supplementation of beta-carotene, retinol, and retinoic acid on phagocyte function during the peripartum period were assessed. Blood was collected at wk -4, -1, 0 (calving), 1, and 4; mammary secretions were collected at wk -1, 0, 1, and 4 from 14 Holstein cows for the isolation of phagocytic cells. Blood polymorphonuclear leukocytes and mammary macrophages and polymorphonuclear leukocytes (phagocytic cells) were assayed for phagocytic and intracellular kill abilities of Staphylococcus aureus in the presence of beta-carotene and retinol at 10(-8) and 10(-7) M and retinoic acid at 10(-9) and 10(-8) M. Phagocytosis by blood or milk phagocytic cells was not influenced by beta-carotene. However, beta-carotene enhanced kill by blood and milk phagocytic cells during certain prepartum and post-partum periods. In contrast to beta-carotene, retinol and retinoic acid either had no effect or suppressed phagocytosis and kill. These results are interpreted to suggest a mechanism by which beta-carotene affords the mammary gland protection against infection, i.e., through enhanced intracellular kill by phagocytes.
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