@article{oliveira_druyan_uni_ashwell_ferket_2013, title={Metabolic profiling of late-term turkey embryos by microarrays}, volume={92}, ISSN={["1525-3171"]}, DOI={10.3382/ps.2012-02354}, abstractNote={The last stages of embryonic development are crucial for turkeys as their metabolism shifts to accommodate posthatch survival and growth. To better understand the metabolic change that occurs during the perinatal period, focused microarray methodology was used to identify changes in the expression of key genes that control metabolism of turkey embryos from 20 d of incubation (E) until hatch (E28). Gene expression patterns were evaluated in liver, pectoral muscle, and hatching muscle and were associated with measured embryonic growth and tissue glycogen concentration. Within the studied period, the expression of 60 genes significantly changed in liver, 53 in pectoral muscle, and 51 in hatching muscle. Genes related to lipid metabolism (enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase, 3-hydroxymethylglutaryl-CoA reductase, acetyl-CoA carboxylase, lipoprotein lipase, and thyroxine deiodinase) had reduced expression between E22 and E26, corresponding to the period of expected limited oxygen supply. In contrast, genes related to opposing pathways in carbohydrate metabolism, such as glycolysis and gluconeogenesis (hexokinases, glucose-6 phosphatase, phosphofructokinases, glucose 1-6 phosphatase, pyruvate kinase, and phosphoenolpyruvate carboxykinase), or glycogenesis and glycogenolysis (glycogen synthase and glycogen phosphorylase) had rather static expression patterns between E22 and E26, indicating their enzymatic activity must be under posttranscriptional control. Metabolic survey by microarray methodology brings new insights into avian embryonic development and physiology.}, number={4}, journal={POULTRY SCIENCE}, author={Oliveira, J. E. and Druyan, S. and Uni, Z. and Ashwell, C. M. and Ferket, P. R.}, year={2013}, month={Apr}, pages={1011–1028} } @article{baurhoo_ferket_ashwell_de oliviera_zhao_2012, title={Cell Walls of Saccharomyces cerevisiae Differentially Modulated Innate Immunity and Glucose Metabolism during Late Systemic Inflammation}, volume={7}, ISSN={1932-6203}, url={http://dx.doi.org/10.1371/journal.pone.0030323}, DOI={10.1371/journal.pone.0030323}, abstractNote={Background Salmonella causes acute systemic inflammation by using its virulence factors to invade the intestinal epithelium. But, prolonged inflammation may provoke severe body catabolism and immunological diseases. Salmonella has become more life-threatening due to emergence of multiple-antibiotic resistant strains. Mannose-rich oligosaccharides (MOS) from cells walls of Saccharomyces cerevisiae have shown to bind mannose-specific lectin of Gram-negative bacteria including Salmonella, and prevent their adherence to intestinal epithelial cells. However, whether MOS may potentially mitigate systemic inflammation is not investigated yet. Moreover, molecular events underlying innate immune responses and metabolic activities during late inflammation, in presence or absence of MOS, are unknown. Methods and Principal Findings Using a Salmonella LPS-induced systemic inflammation chicken model and microarray analysis, we investigated the effects of MOS and virginiamycin (VIRG, a sub-therapeutic antibiotic) on innate immunity and glucose metabolism during late inflammation. Here, we demonstrate that MOS and VIRG modulated innate immunity and metabolic genes differently. Innate immune responses were principally mediated by intestinal IL-3, but not TNF-α, IL-1 or IL-6, whereas glucose mobilization occurred through intestinal gluconeogenesis only. MOS inherently induced IL-3 expression in control hosts. Consequent to LPS challenge, IL-3 induction in VIRG hosts but not differentially expressed in MOS hosts revealed that MOS counteracted LPS's detrimental inflammatory effects. Metabolic pathways are built to elucidate the mechanisms by which VIRG host's higher energy requirements were met: including gene up-regulations for intestinal gluconeogenesis (PEPCK) and liver glycolysis (ENO2), and intriguingly liver fatty acid synthesis through ATP citrate synthase (CS) down-regulation and ATP citrate lyase (ACLY) and malic enzyme (ME) up-regulations. However, MOS host's lower energy demands were sufficiently met through TCA citrate-derived energy, as indicated by CS up-regulation. Conclusions MOS terminated inflammation earlier than VIRG and reduced glucose mobilization, thus representing a novel biological strategy to alleviate Salmonella-induced systemic inflammation in human and animal hosts.}, number={1}, journal={PLoS ONE}, publisher={Public Library of Science (PLoS)}, author={Baurhoo, Bushansingh and Ferket, Peter and Ashwell, Chris M. and de Oliviera, Jean and Zhao, Xin}, editor={Chakravortty, DipshikhaEditor}, year={2012}, month={Jan}, pages={e30323} } @article{de oliveira_druyan_uni_ashwell_ferket_2009, title={Prehatch intestinal maturation of turkey embryos demonstrated through gene expression patterns}, volume={88}, ISSN={0032-5791}, url={http://dx.doi.org/10.3382/ps.2008-00548}, DOI={10.3382/ps.2008-00548}, abstractNote={Some of the challenges faced by neonatal turkeys include weakness, reduced feed intake, impaired growth, susceptibility to disease, and mortality. These symptoms may be due to depleted energy reserves after hatch and an immature digestive system unable to replenish energy reserves from consumed feed. To better understand enteric development in turkeys just before hatch, a new method was used to identify the patterns of intestinal gene expression by utilizing a focused microarray. The duodenums of 24 turkey embryos were sampled on embryonic day (E)20, E24, E26, and hatch (E28). The RNA populations of 96 chosen genes were measured at each time point, from which 81 significantly changed (P < 0.01). These genes were clustered by gene expression pattern similarity into 4 groups. The expression pattern of hormone receptors revealed that intestinal tissues may be less responsive to growth hormone, insulin, glucagon, and triiodothyronine during the last 48 h before hatch, when developmental emphasis switches from cell proliferation to functional maturation. Based on gene expression patterns, we concluded that at hatch, poults should have the capacity to 1) digest disaccharides but not oligopeptides, due to increased expression of sucrase-isomaltase but decreased expression of aminopeptidases and 2) absorb monosaccharides and small peptides due to high expression of sodium-glucose cotransporter-4 and peptide transporter-1.}, number={12}, journal={Poultry Science}, publisher={Elsevier BV}, author={de Oliveira, J.E. and Druyan, S. and Uni, Z. and Ashwell, C.M. and Ferket, P.R.}, year={2009}, month={Dec}, pages={2600–2609} }