scholarly journals 159 Impact of dietary fiber and carbohydrases on intestinal gene transcription in enterotoxigenic E. coli challenged pigs

2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 90-91
Author(s):  
Qingyun Li ◽  
Eric R Burrough ◽  
Nicholas K Gabler ◽  
Stacie A Gould ◽  
Crystal L Loving ◽  
...  
Keyword(s):  
Dietary Fiber ◽  
Gene Transcription ◽  
Intestinal Inflammation ◽  
Random Effect ◽  
Mrna Abundance ◽  
Mrna Levels ◽  
Soluble Fiber ◽  
Barrier Integrity ◽  
E Coli ◽  
Fiber Diet

Abstract This study aimed to evaluate if soluble (10% sugar beet pulp) or insoluble dietary fiber (15% corn DDGS) with or without exogenous carbohydrases protect piglets against enterotoxigenic E. coli (ETEC)-induced changes in gene transcription of markers of intestinal inflammation and barrier integrity. Sixty newly-weaned piglets (BW=6.9 ± 0.1 kg; L337 X Camborough, PIC, Hendersonville, TN) were blocked by initial BW, preselected for F18 ETEC sensitivity and placed in individual pens. Pens were randomly assigned to 1 of 6 treatments (n = 10/trt): non-challenged (NC), ETEC-challenged (PC), PC-fed a soluble fiber diet without (SF-) or with (SF+) carbohydrases (xylanase, β-glucanase, and pectinase), or PC fed an insoluble fiber diet without (IF-) or with carbohydrases (IF+). Pigs were orally inoculated with ETEC or PBS on d 7 post-weaning. Intestinal tissues were collected on d 14 or 15. Data were analyzed using PROC GLIMMIX (SAS 9.4); treatment was a fixed effect and block a random effect. The NC decreased interleukin (IL)-8 and increased claudin-1 (CLDN1; 2.32 vs. 0.96) mRNA abundance in the ileum compared to PC (P < 0.05). The SF- increased ileal CLDN1 mRNA compared to PC (P < 0.05). A trend (P < 0.10) for lower levels of tumor necrosis factor alpha (TNFα) and greater occludin (OCLN) mRNA in the ileum was observed in SF+ compared with PC. The IF+ decreased ileal cluster of differentiation 14 (CD14) mRNA abundance compared to PC (P < 0.05). Greater colonic abundance of zonula occludens (ZO-1) mRNA was observed in NC than PC (P < 0.05). Pigs fed SF+ tended (P = 0.051) to have greater ZO-1 and greater OCLN mRNA abundance than pigs on PC (P < 0.05). Collectively, these data suggest that an ETEC challenge increased markers of gut inflammation and reduced mRNA levels of tight junction proteins. Soluble fiber, regardless of enzyme supplementation, may help improve gut barrier integrity during such a challenge.

The growth hormone-dependent decrease in hepatic fatty acid synthase mRNA is the result of a decrease in gene transcription

1996 ◽  
Vol 16 (2) ◽  
pp. 151-158 ◽  
Author(s):  
S S Donkin ◽  
A D McNall ◽  
B S Swencki ◽  
J L Peters ◽  
T D Etherton
Keyword(s):  
Growth Hormone ◽  
Fatty Acid ◽  
Gene Transcription ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Fatty Acid Synthase ◽  
Hormone Treatment ◽  
Mrna Abundance ◽  
Transcription Rate ◽  
Mrna Levels ◽  
Fas Mrna

ABSTRACT The present study was conducted to determine the chronic effects of porcine growth hormone administration on fatty acid synthase (FAS) mRNA abundance and gene transcription in growing rats. Growth hormone treatment increased growth rate approximately 27% (P<0·01). Porcine growth hormone decreased FAS mRNA levels by 55%. The reduction in FAS mRNA was due to a marked decrease in transcription of the FAS gene (decreased by 80%). In contrast, porcine growth hormone did not affect mRNA abundance or transcription rate of another insulin-regulated gene, phosphoenolpyruvate carboxykinase. In summary, our results have established that chronic treatment with growth hormone decreases FAS mRNA by decreasing the transcription rate of the gene. Furthermore, they suggest that the effects of growth hormone are specific and are not mediated by general changes in insulin-responsive gene expression in liver.

scholarly journals Dietary Indole-3-Carbinol Alleviated Spleen Enlargement, Enhanced IgG Response in C3H/HeN Mice Infected with Citrobacter rodentium

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3148
Author(s):  
Yanbei Wu ◽  
Jing Wang ◽  
Qiang He ◽  
Liangli Yu ◽  
Quynhchi Pham ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Fruits And Vegetables ◽  
Intestinal Inflammation ◽  
Multidrug Resistant ◽  
Enterohemorrhagic Escherichia Coli ◽  
Infection Model ◽  
Mrna Levels ◽  
Citrobacter Rodentium ◽  
E Coli ◽  
Tnf Α

Enteropathogenic and enterohemorrhagic Escherichia coli are important enteric pathogens that induce hemorrhagic colitis or even fatal hemolytic uremic syndrome. Emerging evidence shows that some bio-actives derived from fruits and vegetables may serve as alternatives to antibiotics for overcoming multidrug resistant E. coli infections. In this study, the Citrobacter rodentium (Cr) infection model was utilized to mimic E. coli-induced acute intestinal inflammation, and the effects of a cruciferous vegetable-derived cancer protective compound, indole-3-carbinol (I3C), on the immune responses of Cr-susceptible C3H/HeN mice were investigated. Dietary I3C significantly inhibited the loss of body weight and the increase in spleen size in Cr infected mice. In addition, I3C treatment reduced the inflammatory response to Cr infection by maintaining anti-inflammatory cytokine IL-22 mRNA levels while reducing expression of other pro-inflammatory cytokines including IL17A, IL6, IL1β, TNF-α, and IFN-γ. Moreover, the serum cytokine levels of IL17, TNF-α, IL12p70, and G-CSF also were down-regulated by I3C in Cr-infected mice. Additionally, dietary I3C specifically enhanced the Cr-specific IgG response to Cr infection. In general, dietary I3C reduced the Cr-induced pro-inflammatory response in susceptible C3H/HeN mice and alleviated the physiological changes and tissue damage induced by Cr infection but not Cr colonization.

scholarly journals 132 The impact of F18 ETEC challenge on intestinal integrity and immune response of nursery pigs, and the potential protective effects of direct-fed microbial blends

2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 73-74
Author(s):  
Spenser L Becker ◽  
Qingyun Li ◽  
Eric R Burrough ◽  
John F Patience
Keyword(s):  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Mrna Abundance ◽  
Post Inoculation ◽  
Protective Effects ◽  
Barrier Integrity ◽  
Tlr4 Mrna ◽  
Junction Protein ◽  
Intestinal Barrier Integrity ◽  
The Impact

Abstract The objectives were to investigate the impact of an F18 ETEC challenge on localized immune responses and intestinal function of piglets, and to evaluate potential protective effects of direct-fed microbial blends (DFM1 and DFM2). Thirty-six pens of 3-wk old weaned piglets (2 pigs/pen; BW=6.42 ± 0.22 kg; L337 X Camborough, PIC, Hendersonville, TN) were assigned to one of four treatments: 1) NC: Non-challenged (n = 10), 2) PC:F18 ETEC challenged (n = 10), 3) PC+DFM1 (n = 8) or 4) PC+DFM2 (n = 8). Pigs were either sham-infected with saline or orally challenged with ETEC on d 7 (d 0 post-inoculation, dpi). On dpi 10, ileal mucosa was collected for disaccharidase quantification and whole ileal tissue was collected for immune marker and tight junction protein analysis via qRT-PCR. Data were analyzed using PROC MIXED of SAS (9.4) with dietary treatment as a fixed effect and pen as the experimental unit. There were no differences in lactase activity (P > 0.10). Sucrase and maltase activity increased in PC vs. NC (P < 0.05). Ileal mRNA abundance of zonula occludens-1 (ZO-1) decreased in PC and DFM1 compared with NC (P < 0.05). DFM2 increased ZO-1 compared with PC (P < 0.05). There was no difference in claudin-1 mRNA (P > 0.10). Cluster of differentiation 14 (CD14) mRNA was elevated in challenged pigs compared with NC (P < 0.05). Interleukin-10 (IL-10) tended to be elevated in both DFM treatments compared with PC (P < 0.10). All challenged treatments tended to have elevated tumor necrosis factor-a (TNFa) abundance vs. NC (P < 0.10). There were no differences in IL-1b, IL-6, or toll-like receptor 4 (TLR4) mRNA abundance (P > 0.10). In conclusion, the ETEC challenge increased CD14, tended to increase TNFa, and decreased ZO-1 mRNA abundance, indicating activation of intestinal inflammation and impaired intestinal barrier integrity. DFM2 may improve intestinal barrier integrity impaired by ETEC as evidenced by increased ZO-1 mRNA.

scholarly journals High-fat diet intake modulates maternal intestinal adaptations to pregnancy, and results in placental hypoxia and impaired fetal gut development

2018 ◽  
Author(s):  
Wajiha Gohir ◽  
Katherine M. Kennedy ◽  
Jessica G. Wallace ◽  
Michelle Saoi ◽  
Christian J. Bellissimo ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Health Research ◽  
High Fat Diet ◽  
Intestinal Inflammation ◽  
Mrna Levels ◽  
Gut Development ◽  
High Fat ◽  
Gut Barrier ◽  
Barrier Integrity ◽  
Diet Intake

Shifts in maternal intestinal microbiota have been implicated in metabolic adaptations to pregnancy. In this study we investigated how high-fat diet intake impacts the maternal gut microbiota, intestinal inflammation and gut barrier integrity, placental inflammation, and fetal intestinal development at E18.5. High-fat diet (HFD) was associated with decreased relative abundancesof SCFA producing genera during pregnancy. These diet-induced shifts paralleled decreased maternal intestinal mRNA levels of SCFA receptor Gpr41, modestly decreased cecal butyrate, and altered mRNA levels of inflammatory cytokines and immune cell markers in the maternal intestine. Maternal HFD resulted inimpaired gut barrier integrity, with corresponding increases in circulating maternal levels of LPS and TNF.Placentafromhigh-fat fed damsdemonstrated blood vessel immatu-rityand hypoxia, decreased freecarnitine, acylcarnitine derivatives, TMAO, as well as altered mRNA levels of inflammation, autophagy and ER stress markers. HFD exposed fetuses had increased activation of NF-κB and inhibition of the unfolded protein response in the developing intestine. Together, these data suggest that high-fat diet intake prior to and during pregnancy shifts the composition of the maternal gut microbiota and impairs gut barrier integrity, resulting in increased maternal circulating LPS, which may ultimate contribute to changes in placental vasculariza-tion and fetal gut development.Funding informationFarncombe Family Digestive Health Research Institute (KMK); Canadian Institute of Health Research (CJB); Canada Research Chairs Program (MGS, DMS); Natural Sciences and Engineering Research Council of Canada, Genome Canada (PBM).

scholarly journals Distribution of Lactoferrin Is Related with Dynamics of Neutrophils in Bacterial Infected Mice Intestine

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1496 ◽  
Author(s):  
Li Liang ◽  
Zhen-Jie Wang ◽  
Guang Ye ◽  
Xue-You Tang ◽  
Yuan-Yuan Zhang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Antimicrobial Activity ◽  
Mucosal Immunity ◽  
Mrna Levels ◽  
Iron Binding ◽  
E Coli ◽  
New Knowledge ◽  
Activated Neutrophils ◽  
Binding Glycoprotein

Lactoferrin (Lf) is a conserved iron-binding glycoprotein with antimicrobial activity, which is present in secretions that recover mucosal sites regarded as portals of invaded pathogens. Although numerous studies have focused on exogenous Lf, little is known about its expression of endogenous Lf upon bacterial infection. In this study, we investigated the distribution of Lf in mice intestine during Escherichia coli (E. coli) K88 infection. PCR and immunohistology staining showed that mRNA levels of Lf significantly increased in duodenum, ileum and colon, but extremely decreased in jejunum at 8 h and 24 h after infection. Meanwhile, endogenous Lf was mostly located in the lamina propria of intestine villi, while Lf receptor (LfR) was in the crypts. It suggested that endogenous Lf-LfR interaction might not be implicated in the antibacterial process. In addition, it was interesting to find that the infiltration of neutrophils into intestine tissues was changed similarly to Lf expression. It indicated that the variations of Lf expression were rather due to an equilibrium between the recruitment of neutrophils and degranulation of activated neutrophils. Thus, this new knowledge will pave the way to a more effective understanding of the role of Lf in intestinal mucosal immunity.

Nitric oxide increases IL-8 gene transcription and mRNA stability to enhance IL-8 gene expression in lung epithelial cells

2004 ◽  
Vol 287 (4) ◽  
pp. L764-L773 ◽  
Author(s):  
Loretta Sparkman ◽  
Vijayakumar Boggaram
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Gene Transcription ◽  
Mrna Stability ◽  
Inflammatory Responses ◽  
Lung Epithelial Cells ◽  
Mrna Levels ◽  
Lung Epithelial

Interleukin (IL)-8, a C-X-C chemokine, is a potent chemoattractant and an activator for neutrophils, T cells, and other immune cells. The airway and respiratory epithelia play important roles in the initiation and modulation of inflammatory responses via production of cytokines and surfactant. The association between elevated levels of nitric oxide (NO) and IL-8 in acute lung injury associated with sepsis, acute respiratory distress syndrome, respiratory syncytial virus infection in infants, and other inflammatory diseases suggested that NO may play important roles in the control of IL-8 gene expression in the lung. We investigated the role of NO in the control of IL-8 gene expression in H441 lung epithelial cells. We found that a variety of NO donors significantly induced IL-8 mRNA levels, and the increase in IL-8 mRNA was associated with an increase in IL-8 protein. NO induction of IL-8 mRNA was due to increases in IL-8 gene transcription and mRNA stability. NO induction of IL-8 mRNA levels was not inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and KT-5823, inhibitors of soluble guanylate cyclase and protein kinase G, respectively, and 8-bromo-cGMP did not increase IL-8 mRNA levels. This indicated that NO induces IL-8 mRNA levels independently of changes in the intracellular cGMP levels. NO induction of IL-8 mRNA was significantly reduced by inhibitors of extracellular regulated kinase and protein kinase C. IL-8 induction by NO was also reduced by hydroxyl radical scavengers such as dimethyl sulfoxide and dimethylthiourea, indicating the involvement of hydroxyl radicals in the induction process. NO induction of IL-8 gene expression could be a significant contributing factor in the initiation and induction of inflammatory response in the respiratory epithelium.

Abdominal irradiation increases inflammatory cytokine expression and activates NF-κB in rat ileal muscularis layer

2003 ◽  
Vol 285 (3) ◽  
pp. G556-G565 ◽  
Author(s):  
C. Linard ◽  
A. Ropenga ◽  
M. C. Vozenin-Brotons ◽  
A. Chapel ◽  
D. Mathe
Keyword(s):  
Inflammatory Cytokine ◽  
Intestinal Inflammation ◽  
Clinical Symptoms ◽  
Early Stage ◽  
Cytokine Expression ◽  
Mrna Levels ◽  
Activator Protein 1 ◽  
Γ Irradiation ◽  
Control Tissue ◽  
Anti Inflammatory

The small bowel is an important dose-limiting organ in abdominal radiotherapy because irradiation can cause acute enteritis that, in turn, leads to progressively reduced motility and finally, in a later phase, to fibrosis. Because these clinical symptoms may be caused by the early stage of an inflammatory process, we characterized the radiation-induced intestinal inflammation in rats. Abdominal γ-irradiation (10-Gy) induced a cascade of inflammatory events characterized by an early (6 h after exposure) increase in IL-1β, TNF-α, and IL-6 mRNA levels in the rat ileal muscularis layer. IL-8 [a cytokine-induced neutrophil chemoattractant (CINC)] mRNA appeared later (at 3 days). The expression of TGF-β (a profibrotic cytokine) was higher in irradiated than control tissue at day 1, whereas IL-10 (an anti-inflammatory cytokine) expression vanished completely. Despite strong IL-1ra expression, the IL-1ra/IL-1β ratio, which is an indicator of inflammatory balance, was -41% at day 1 in irradiated compared with control tissue. The nuclear transcription factors NF-κB and activator protein-1 (AP-1) govern transcription of these genes, directly or indirectly. Although expression of the subunits of NF-κB (p65, p50) and AP-1 (c- fos, c- jun) did not increase, irradiation caused a rapid and persistent translocation of p65 and p50. An imbalance between proinflammatory and anti-inflammatory mediators may contribute to perpetuating intestinal inflammation, thus making it chronic.

The Corfu δβ thalassemia deletion disrupts γ-globin gene silencing and reveals post-transcriptional regulation of HbF expression

Blood ◽  
2005 ◽  
Vol 105 (5) ◽  
pp. 2154-2160 ◽  
Author(s):  
Lyubomira Chakalova ◽  
Cameron S. Osborne ◽  
Yan-Feng Dai ◽  
Beatriz Goyenechea ◽  
Anna Metaxotou-Mavromati ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Gene Transcription ◽  
Globin Gene ◽  
Fetal Hemoglobin ◽  
Critical Threshold ◽  
Critical Element ◽  
Mrna Levels ◽  
Globin Genes ◽  
Mrna Accumulation ◽  
Post Transcriptional Regulation

Abstract The 7.2 kilobase (kb) Corfu δβ thalassemia mutation is the smallest known deletion encompassing a region upstream of the human δ gene that has been suggested to account for the vastly different phenotypes in hereditary persistence of fetal hemoglobin (HPFH) versus β thalassemia. Fetal hemoglobin (HbF) expression in Corfu heterozygotes and homozygotes is paradoxically dissimilar, suggesting conflicting theories as to the function of the region on globin gene regulation. Here, we measure γ- and β-globin gene transcription, steady-state mRNA, and hemoglobin expression levels in primary erythroid cells cultured from several patients with Corfu δβ thalassemia. We show through RNA fluorescence in situ hybridization that the Corfu deletion results in high-level transcription of the fetal γ genes in cis with a concomitant reduction in transcription of the downstream β gene. Surprisingly, we find that elevated γ gene transcription does not always result in a corresponding accumulation of γ mRNA or fetal hemoglobin, indicating a post-transcriptional regulation of γ gene expression. The data suggest that efficient γ mRNA accumulation and HbF expression are blocked until β mRNA levels fall below a critical threshold. These results explain the Corfu paradox and show that the deleted region harbors a critical element that functions in the developmentally regulated transcription of the β-globin genes.

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