60 The Effect of Neomycin Inclusion in Milk Replacer on Gut Health and Development in Preweaned Male Holstein Calves

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 33-34
Author(s):  
Lauralise Buss ◽  
Taylor Yohe ◽  
Lautaro Rostoll Cangiano ◽  
Aaron Keunen ◽  
Leluo Guan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Early Life ◽  
Gut Health ◽  
Gut Development ◽  
Gut Permeability ◽  
Junction Protein ◽  
Health And Development ◽  
Distal Jejunum ◽  
Total Bacteria

Abstract Neomycin is commonly used in calf milk replacers (MR) to prevent diarrhea, however, antimicrobial exposure in early life may have consequences to gut development. The objective of this study was to investigate the effects of neomycin inclusion in MR on calf gut health and development. Thirty-six calves were randomly assigned to one of three treatments: control (CON), non-medicated (MR, n = 12), short-term antimicrobial exposure (ST: 20 mg/kg BW neomycin mixed in MR from d 1–14, n = 12), or long-term antimicrobial exposure (LT: 20 mg/kg BW neomycin in MR from d 1–28, n = 12). Fecal samples were collected weekly to measure total bacteria, and gut permeability was measured in week 2 and 4 by comparing serum recovery of orally dosed lactulose and D-mannitol markers. Calves were dissected at week 5 to collect intestinal tissues, which were used to analyze histology, gene expression and total bacteria abundance. Digesta samples were collected to analyze for total bacteria abundance and volatile fatty acid (VFA) concentrations. No treatment effects were found in the amounts of total bacteria in fecal, digesta, or tissue samples. Marker recovery in serum was higher at week 2 compared to week 4 (P < 0.01), suggesting that calves in early life have higher gut permeability. Histomorphological measures were similar, except for villi length in the distal jejunum, which was longest in ST calves (P = 0.05). Tight-junction, mucus, and inflammatory-associated gene expression was similar overall, although the expression of Tight junction protein-1 in the distal jejunum was lowest in CON calves (P = 0.04). Distal jejunum acetic acid, propionic acid, and total VFA tended to be highest in LT calves (P = 0.09; P = 0.06; P = 0.07, respectively). Although this study found few consequences of neomycin to gut health, the lack of benefits supports the argument that antimicrobials should be used prudently.

The Tight Junction Protein Cingulin Regulates Gene Expression and RhoA Signaling

2009 ◽  
Vol 1165 (1) ◽  
pp. 88-98 ◽  
Author(s):  
Sandra Citi ◽  
Serge Paschoud ◽  
Pamela Pulimeno ◽  
Francesco Timolati ◽  
Fabrizio De Robertis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Tight Junction Protein ◽  
Junction Protein ◽  
Rhoa Signaling

scholarly journals Sex differences in stroke outcome correspond to rapid and severe changes in gut permeability in adult Sprague-Dawley rats

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yumna El-Hakim ◽  
Kathiresh Kumar Mani ◽  
Amir Eldouh ◽  
Sivani Pandey ◽  
Maria T. Grimaldo ◽  
...  
Keyword(s):  
Sex Differences ◽  
Tight Junction ◽  
Infarct Volume ◽  
Motor Impairment ◽  
Gut Permeability ◽  
Sprague Dawley ◽  
Stroke Outcomes ◽  
Sprague Dawley Rats ◽  
Junction Protein ◽  
Sensory Motor

Abstract Background Sex differences in experimental stroke outcomes are well documented, such that adult males have a greater infarct volume, increased stroke-induced mortality, and more severe sensory-motor impairment. Based on recent evidence that the gut is an early responder to stroke, the present study tested the hypothesis that sex differences in stroke severity will be accompanied by rapid and greater permeability of the gut-blood barrier and gut dysbiosis in males as compared to females. Method Male and female Sprague-Dawley rats (5–7 months of age) were subject to endothelin (ET)-1-induced middle cerebral artery occlusion (MCAo). Sensory-motor tests were conducted pre- and 2 days after MCAo. Gut permeability was assessed in serum samples using biomarkers of gut permeability as well as functional assays using size-graded dextrans. Histological analysis of the gut was performed with H&E staining, periodic acid-Schiff for mucus, and immunohistochemistry for the tight junction protein, ZO-1. Fecal samples obtained pre- and post-stroke were analyzed for bacterial taxa and short-chain fatty acids (SCFAs). Results After stroke, males displayed greater mortality, worse sensory-motor deficit, and higher serum levels of proinflammatory cytokines IL-17A, MCP-1, and IL-5 as compared to females. MCAo-induced gut permeability was rapid and severe in males as indicated by dextran extravasation from the gut to the blood in the hyperacute (< 2 h) and early acute (2 days) phase of stroke. This was accompanied by dysmorphology of the gut villi and dysregulation of the tight junction protein ZO-1 in the acute phase. Fecal 16s sequencing showed no differences in bacterial diversity in the acute phase of stroke. Predictive modeling indicated that markers of gut permeability were associated with acute sensory-motor impairment and infarct volume. Conclusions These data show that extensive leakiness of the gut barrier is associated with severe post-stroke disability and suggest that reinforcing this barrier may improve stroke outcomes.

scholarly journals PSIII-18 Assessment of Salmonella Dublin infection of intestinal porcine epithelial cells (IPEC) in response to Zinc Oxide and a Yeast Mannan Rich Fraction

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 365-366
Author(s):  
Niall Browne ◽  
Seána Jordan ◽  
Karina Horgan
Keyword(s):  
Gene Expression ◽  
Zinc Oxide ◽  
Tight Junction ◽  
Control Cell ◽  
Bacterial Attachment ◽  
Intestinal Cell ◽  
Gut Health ◽  
Suitable Alternative ◽  
Salmonella Dublin

Abstract Salmonella species are associated with post-weaning diarrhea, which results in poor weight gain, potential death, and economic cost. A yeast mannan rich fraction (MRF) was assessed alongside the industry standard treatment Zinc Oxide (ZO) in vitro to determine its impact on Salmonella Dublin infection of a pig intestinal cell line (IPEC). IPEC cells were exposed to MRF or ZO in the presence of S. Dublin (1x108/mL). IPEC cell RNA was isolated and cDNA synthesized. Gene expression for IL-1β, TNFα, IL-8 and cellular tight Junction genes Occludin, Claudin3 and Tight junction protein1 (TJP1) were assessed by qPCR. S. Dublin adhesion to IPEC cells (500:1) assessed in the presence or absence of either ZO or MRF for 1 hour at 37°C. IPEC cells with attached S. Dublin were lysed, diluted, plated and incubated overnight and enumeration. Three biological replicates were performed for all experiments and statistical analysis determined by One-way ANOVA. Proinflammatory gene TNFα was significantly reduced (P ≤ 0.001) following S. Dublin infection and treatment with MRF compared with ZO. IL-1β demonstrated no change between treatments although IL-8 gene expression was significantly reduced in both ZO (P≤0.01) and MRF (P ≤ 0.05) treated cells over the control. Significantly higher expression of Occludin (P ≤ 0.01), Claudin3 (P ≤ 0.001) and TJP1 (P ≤ 0.05) was observed in IPEC cells exposed to S. Dublin in the presence of MRF compared to ZO. Adhesion of S. Dublin to IPEC cells was significantly reduced in response to MRF addition compared to ZO treated cells (P ≤ 0.001) and the control cells (P ≤ 0.05). ZO treated cell demonstrated no improvement over the control cell levels of bacterial attachment. Both on a physical and molecular level bacterial infection of intestinal cells was more significantly impaired by MRF addition. With the ban on ZO, yeast MRF may prove to be a suitable alternative to support gut health in piglets.

scholarly journals Optimal liver metabolism and proliferation require the tight junction protein claudin-3

2021 ◽  
Vol 108 (Supplement_4) ◽  
Author(s):  
F A Baier ◽  
D Sanchez-Taltavull ◽  
C Gómez Castellà ◽  
F Jebbawi ◽  
A Keogh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Energy Homeostasis ◽  
Transmembrane Protein ◽  
Parenchymal Cell ◽  
Cell Cycle Gene ◽  
Tight Junction Proteins ◽  
Specific Expression ◽  
Junction Protein ◽  
Junction Proteins

Abstract Objective The expression of hepatic tight junction proteins and their contribution to homeostasis and regeneration remained largely unexplored. Here, we determine the cell type specific expression of tight junction genes in murine livers. We further explore the regulation and functional importance of the transmembrane protein CLDN3 in normal and regenerating livers. Methods Murine livers were used for tissue- and single cell RNA-seq. CLDN3 localization was determined by immunofluorescence. CLDN3+/+ or CLDN3-/- livers were analysed by electron microscopy, fluorescence-activated cell sorting and liquid chromatography mass spectrometry. Lipid content was quantified with oil-red. Mice were subjected to 2/3 partial hepatectomy. Proliferation was quantified with Ki67 and pHH3 stainings. Cell cycle gene expression was determined by RT-qPCR. Barrier impairments were assessed with total bile acid measurements. Differential gene expression was analysed by tissue RNAseq with DESeq2. Results We determined the profile of tight junction gene expression the main liver cell types, showing that tight junction transcripts can be found in hepatocytes and cholangiocytes but also on non-parenchymal cell populations. CLDN3 was among the highly expressed- and regulated genes in native and regenerating livers. CLDN3 had a zonated expression pattern. CLDN3-/- mice had microscopically intact tight junctions, but showed significantly downregulated hepatic energy metabolism and suboptimal cell proliferation in the regeneration model. Conclusion Our data suggests a functional role of CLDN3 for maintenance of energy homeostasis and optimal regeneration, proving that the function of hepatic tight junction proteins extends beyond basic membrane sealing.

ZO-2, a tight junction protein involved in gene expression, proliferation, apoptosis, and cell size regulation

2017 ◽  
Vol 1397 (1) ◽  
pp. 35-53 ◽  
Author(s):  
Lorenza González-Mariscal ◽  
Jael Miranda ◽  
Arturo Raya-Sandino ◽  
Alaide Domínguez-Calderón ◽  
Francisco Cuellar-Perez
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Cell Size ◽  
Tight Junction Protein ◽  
Size Regulation ◽  
Junction Protein

scholarly journals MicroRNA Regulation of Endothelial Junction Proteins and Clinical Consequence

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Yugang Zhuang ◽  
Hu Peng ◽  
Victoria Mastej ◽  
Weiguo Chen
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Focal Adhesion ◽  
Protein Gene ◽  
Mirna Regulation ◽  
Adhesion Junctions ◽  
Junction Protein ◽  
Cellular Junctions ◽  
Junction Structure ◽  
Junction Proteins

Cellular junctions play a critical role in structural connection and signal communication between cells in various tissues. Although there are structural and functional varieties, cellular junctions include tight junctions, adherens junctions, focal adhesion junctions, and tissue specific junctions such as PECAM-1 junctions in endothelial cells (EC), desmosomes in epithelial cells, and hemidesmosomes in EC. Cellular junction dysfunction and deterioration are indicative of clinical diseases. MicroRNAs (miRNA) are ~20 nucleotide, noncoding RNAs that play an important role in posttranscriptional regulation for almost all genes. Unsurprisingly, miRNAs regulate junction protein gene expression and control junction structure integrity. In contrast, abnormal miRNA regulation of junction protein gene expression results in abnormal junction structure, causing related diseases. The major components of tight junctions include zonula occluden-1 (ZO-1), claudin-1, claudin-5, and occludin. The miRNA regulation of ZO-1 has been intensively investigated. ZO-1 and other tight junction proteins such as claudin-5 and occludin were positively regulated by miR-126, miR-107, and miR21 in different models. In contrast, ZO-1, claudin-5, and occludin were negatively regulated by miR-181a, miR-98, and miR150. Abnormal tight junction miRNA regulation accompanies cerebral middle artery ischemia, brain trauma, glioma metastasis, and so forth. The major components of adherens junctions include VE-cadherin, β-catenin, plakoglobin, P120, and vinculin. VE-cadherin and β-catenin were regulated by miR-9, miR-99b, miR-181a, and so forth. These regulations directly affect VE-cadherin-β-catenin complex stability and further affect embryo and tumor angiogenesis, vascular development, and so forth. miR-155 and miR-126 have been shown to regulate PECAM-1 and affect neutrophil rolling and EC junction integrity. In focal adhesion junctions, the major components are integrin β4, paxillin, and focal adhesion kinase (FAK). Integrin β4 has been regulated by miR-184, miR-205, and miR-9. Paxillin has been regulated by miR-137, miR-145, and miR-218 in different models. FAK has been regulated by miR-7, miR-138, and miR-135. Deregulation of miRNAs is caused by viral infections, tumorigenesis, and so forth. By regulation of posttranscription, miRNAs manipulate junction protein expression in all cellular processes and further determine cellular fate and development. Elucidation of these regulatory mechanisms will become a new alternative therapy for many diseases, such as cancers and inflammatory diseases.

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