Database : MEDLINE
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[PMID]: 29522566
[Au] Autor:Zhang K; Riba A; Nietschke M; Torow N; Repnik U; Pütz A; Fulde M; Dupont A; Hensel M; Hornef M
[Ad] Address:Institute of Medical Microbiology, RWTH University Hospital, Aachen, Germany.
[Ti] Title:Minimal SPI1-T3SS effector requirement for Salmonella enterocyte invasion and intracellular proliferation in vivo.
[So] Source:PLoS Pathog;14(3):e1006925, 2018 Mar 09.
[Is] ISSN:1553-7374
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Effector molecules translocated by the Salmonella pathogenicity island (SPI)1-encoded type 3 secretion system (T3SS) critically contribute to the pathogenesis of human Salmonella infection. They facilitate internalization by non-phagocytic enterocytes rendering the intestinal epithelium an entry site for infection. Their function in vivo has remained ill-defined due to the lack of a suitable animal model that allows visualization of intraepithelial Salmonella. Here, we took advantage of our novel neonatal mouse model and analyzed various bacterial mutants and reporter strains as well as gene deficient mice. Our results demonstrate the critical but redundant role of SopE2 and SipA for enterocyte invasion, prerequisite for transcriptional stimulation and mucosal translocation in vivo. In contrast, the generation of a replicative intraepithelial endosomal compartment required the cooperative action of SipA and SopE2 or SipA and SopB but was independent of SopA or host MyD88 signaling. Intraepithelial growth had no critical influence on systemic spread. Our results define the role of SPI1-T3SS effector molecules during enterocyte invasion and intraepithelial proliferation in vivo providing novel insight in the early course of Salmonella infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1371/journal.ppat.1006925

  2 / 8594 MEDLINE  
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[PMID]: 29471144
[Au] Autor:Tao W; Zhao D; Sun M; Wang Z; Lin B; Bao Y; Li Y; He Z; Sun Y; Sun J
[Ad] Address:Wuya College of Innovation, Shenyang Pharmaceutical University, No. 103 Wenhua Road, Shenyang 110016, China.
[Ti] Title:Intestinal absorption and activation of decitabine amino acid ester prodrugs mediated by peptide transporter PEPT1 and enterocyte enzymes.
[So] Source:Int J Pharm;541(1-2):64-71, 2018 Feb 19.
[Is] ISSN:1873-3476
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Decitabine (DAC), a potent DNA methyltransferase (DNMT) inhibitor, has a limited oral bioavailability. Its 5'-amino acid ester prodrugs could improve its oral delivery but the specific absorption mechanism is not yet fully understood. The aim of this present study was to investigate the in vivo absorption and activation mechanism of these prodrugs using in situ intestinal perfusion and pharmacokinetics studies in rats. Although PEPT1 transporter is pH dependent, there appeared to be no proton cotransport in the perfusion experiment with a preferable transport at pH 7.4 rather than pH 6.5. This suggested that the transport was mostly dependent on the dissociated state of the prodrugs and the proton gradient might play only a limited role. In pH 7.4 HEPES buffer, an increase in P was observed for L-val-DAC, D-val-DAC, L-phe-DAC and L-trp-DAC (2.89-fold, 1.2-fold, 2.73-fold, and 1.90-fold, respectively), compared with the parent drug. When co-perfusing the prodrug with Glysar, a known substrate of PEPT1, the permeabilities of the prodrugs were significantly inhibited compared with the control. To further investigate the absorption of the prodrugs, L-val-DAC was selected and found to be concentration-dependent and saturable, suggesting a carrier-mediated process (intrinsic K : 7.80 ±â€¯2.61 mM) along with passive transport. Determination of drug in intestinal homogenate after perfusion further confirmed that the metabolic activation mainly involved an intestinal first-pass effect. In a pharmacokinetic evaluation, the oral bioavailability of L-val-DAC, L-phe-DAC and L-trp-DAC were nearly 1.74-fold, 1.69-fold and 1.49-fold greater than that of DAC. The differences in membrane permeability and oral bioavailability might be due to the different stability in the intestinal lumen and the distinct PEPT1 affinity which is mainly caused by the stereochemistry, hydrophobicity and steric hindrance of the side chains. In summary, the detailed investigation of the absorption mechanism by in vivo intestinal perfusion and pharmacokinetic studies showed that the prodrugs of DAC exhibited excellent permeability and oral bioavailability, which might be attributed to a hybrid (partly PEPT1-mediated and partly passive) transport mode and a rapid activation process in enterocytes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  3 / 8594 MEDLINE  
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[PMID]: 29317503
[Au] Autor:Lopes F; Keita ÅV; Saxena A; Reyes JL; Mancini NL; Al Rajabi A; Wang A; Baggio CH; Dicay M; van Dalen R; Ahn Y; Carneiro MBH; Peters NC; Rho JM; MacNaughton WK; Girardin SE; Jijon H; Philpott DJ; Söderholm JD; McKay DM
[Ad] Address:From the Gastrointestinal Research Group, Departments of Physiology and Pharmacology and flopes77@gmail.com.
[Ti] Title:ER-stress mobilization of death-associated protein kinase-1-dependent xenophagy counteracts mitochondria stress-induced epithelial barrier dysfunction.
[So] Source:J Biol Chem;293(9):3073-3087, 2018 Mar 02.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The gut microbiome contributes to inflammatory bowel disease (IBD), in which bacteria can be present within the epithelium. Epithelial barrier function is decreased in IBD, and dysfunctional epithelial mitochondria and endoplasmic reticulum (ER) stress have been individually associated with IBD. We therefore hypothesized that the combination of ER and mitochondrial stresses significantly disrupt epithelial barrier function. Here, we treated human colonic biopsies, epithelial colonoids, and epithelial cells with an uncoupler of oxidative phosphorylation, dinitrophenol (DNP), with or without the ER stressor tunicamycin and assessed epithelial barrier function by monitoring internalization and translocation of commensal bacteria. We also examined barrier function and colitis in mice exposed to dextran sodium sulfate (DSS) or DNP and co-treated with DAPK6, an inhibitor of death-associated protein kinase 1 (DAPK1). Contrary to our hypothesis, induction of ER stress ( the unfolded protein response) protected against decreased barrier function caused by the disruption of mitochondrial function. ER stress did not prevent DNP-driven uptake of bacteria; rather, specific mobilization of the ATF6 arm of ER stress and recruitment of DAPK1 resulted in enhanced autophagic killing (xenophagy) of bacteria. Of note, epithelia with a Crohn's disease-susceptibility mutation in the autophagy gene exhibited less xenophagy. Systemic delivery of the DAPK1 inhibitor DAPK6 increased bacterial translocation in DSS- or DNP-treated mice. We conclude that promoting ER stress-ATF6-DAPK1 signaling in transporting enterocytes counters the transcellular passage of bacteria evoked by dysfunctional mitochondria, thereby reducing the potential for metabolic stress to reactivate or perpetuate inflammation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.RA117.000809

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[PMID]: 29514136
[Au] Autor:Park JS; Jeon HJ; Pyo JH; Kim YS; Yoo MA
[Ad] Address:Department of Molecular Biology, Pusan National University, Busan 46241, Republic of Korea.
[Ti] Title:Deficiency in DNA damage response of enterocytes accelerates intestinal stem cell aging in .
[So] Source:Aging (Albany NY);, 2018 Mar 07.
[Is] ISSN:1945-4589
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Stem cell dysfunction is closely linked to tissue and organismal aging and age-related diseases, and heavily influenced by the niche cells' environment. The DNA damage response (DDR) is a key pathway for tissue degeneration and organismal aging; however, the precise protective role of DDR in stem cell/niche aging is unclear. The midgut is an excellent model to study the biology of stem cell/niche aging because of its easy genetic manipulation and its short lifespan. Here, we showed that deficiency of DDR in enterocytes (ECs) accelerates intestinal stem cell (ISC) aging. We generated flies with knockdown of , , , , , , and , which decrease the DDR system in ECs. EC-specific DDR depletion induced EC death, accelerated the aging of ISCs, as evidenced by ISC hyperproliferation, DNA damage accumulation, and increased centrosome amplification, and affected the adult fly's survival. Our data indicated a distinct effect of DDR depletion in stem or niche cells on tissue-resident stem cell proliferation. Our findings provide evidence of the essential role of DDR in protecting EC against ISC aging, thus providing a better understanding of the molecular mechanisms of stem cell/niche aging.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.18632/aging.101390

  5 / 8594 MEDLINE  
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[PMID]: 29432213
[Au] Autor:Mulvihill EE
[Ad] Address:University of Ottawa Heart Institute, University of Ottawa, Department of Biochemistry, Microbiology and Immunology, Ottawa, Ontario, Canada.
[Ti] Title:Regulation of intestinal lipid and lipoprotein metabolism by the proglucagon-derived peptides glucagon like peptide 1 and glucagon like peptide 2.
[So] Source:Curr Opin Lipidol;29(2):95-103, 2018 Apr.
[Is] ISSN:1473-6535
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:PURPOSE OF REVIEW: The intestine is highly efficient at absorbing and packaging dietary lipids onto the structural protein apoB48 for distribution throughout the body. Here, we summarize recent advances into understanding the physiological and pharmacological actions of the proglucagon-derived peptides: glucagon like peptide 1 (GLP-1) and glucagon like peptide 2 (GLP-2) on intestinal lipoprotein secretion. RECENT FINDINGS: Several recent studies have elucidated mechanisms underlying the paradoxical effects of GLP-1 and GLP-2 on intestinal production of triglyceride-rich lipoproteins (TRLs). Both gut-derived peptides are secreted on an equimolar basis in response to the same nutrient stimulus. Despite neither receptor demonstrating clear localization to enterocytes, a single injection of a GLP-1R agonist rapidly decreases delivery of intestinally packaged fatty acids into the plasma, while conversely GLP-2 receptor (GLP-2R) activation acutely increases TRL concentrations in plasma. SUMMARY: The regulation of TRL secretion is dependent on the coordination of many processes: fatty acid availability uptake, assembly onto the apoB48 polypeptide backbone, secretion and reuptake, which the hormonal, neural, inflammatory and metabolic milieu can all strongly influence. Understanding of how GLP-1 and GLP-2 receptor agonists control TRL production has clinical importance given that GLP1R agonists were recently demonstrated not only to provide glycemic control but also to prevent major adverse cardiovascular events in patients with T2DM and the success of GLP-2R agonists in treating short bowel disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1097/MOL.0000000000000495

  6 / 8594 MEDLINE  
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[PMID]: 29361088
[Au] Autor:Haberman Y; BenShoshan M; Di Segni A; Dexheimer PJ; Braun T; Weiss B; Walters TD; Baldassano RN; Noe JD; Markowitz J; Rosh J; Heyman MB; Griffiths AM; Crandall WV; Mack DR; Baker SS; Kellermayer R; Patel A; Otley A; Steiner SJ; Gulati AS; Guthery SL; LeLeiko N; Moulton D; Kirschner BS; Snapper S; Avivi C; Barshack I; Oliva-Hemker M; Cohen SA; Keljo DJ; Ziring D; Anikster Y; Aronow B; Hyams JS; Kugathasan S; Denson LA
[Ad] Address:Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
[Ti] Title:Long ncRNA Landscape in the Ileum of Treatment-Naive Early-Onset Crohn Disease.
[So] Source:Inflamm Bowel Dis;24(2):346-360, 2018 Jan 18.
[Is] ISSN:1536-4844
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Background: Long noncoding RNAs (lncRNA) are key regulators of gene transcription and many show tissue-specific expression. We previously defined a novel inflammatory and metabolic ileal gene signature in treatment-naive pediatric Crohn disease (CD). We now extend our analyses to include potential regulatory lncRNA. Methods: Using RNAseq, we systematically profiled lncRNAs and protein-coding gene expression in 177 ileal biopsies. Co-expression analysis was used to identify functions and tissue-specific expression. RNA in situ hybridization was used to validate expression. Real-time polymerase chain reaction was used to test lncRNA regulation by IL-1ß in Caco-2 enterocytes. Results: We characterize widespread dysregulation of 459 lncRNAs in the ileum of CD patients. Using only the lncRNA in discovery and independent validation cohorts showed patient classification as accurate as the protein-coding genes, linking lncRNA to CD pathogenesis. Co-expression and functional annotation enrichment analyses across several tissues and cell types 1showed that the upregulated LINC01272 is associated with a myeloid pro-inflammatory signature, whereas the downregulated HNF4A-AS1 exhibits association with an epithelial metabolic signature. We confirmed tissue-specific expression in biopsies using in situ hybridization, and validated regulation of prioritized lncRNA upon IL-1ß exposure in differentiated Caco-2 cells. Finally, we identified significant correlations between LINC01272 and HNF4A-AS1 expression and more severe mucosal injury. Conclusions: We systematically define differentially expressed lncRNA in the ileum of newly diagnosed pediatric CD. We show lncRNA utility to correctly classify disease or healthy states and demonstrate their regulation in response to an inflammatory signal. These lncRNAs, after mechanistic exploration, may serve as potential new tissue-specific targets for RNA-based interventions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1093/ibd/izx013

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[PMID]: 29507250
[Au] Autor:Hudson BH; Hale AT; Irving RP; Li S; York JD
[Ad] Address:Department of Biochemistry, Vanderbilt University, Nashville, TN 37232.
[Ti] Title:Modulation of intestinal sulfur assimilation metabolism regulates iron homeostasis.
[So] Source:Proc Natl Acad Sci U S A;, 2018 Mar 05.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Sulfur assimilation is an evolutionarily conserved pathway that plays an essential role in cellular and metabolic processes, including sulfation, amino acid biosynthesis, and organismal development. We report that loss of a key enzymatic component of the pathway, bisphosphate 3'-nucleotidase (Bpnt1), in mice, both whole animal and intestine-specific, leads to iron-deficiency anemia. Analysis of mutant enterocytes demonstrates that modulation of their substrate 3'-phosphoadenosine 5'-phosphate (PAP) influences levels of key iron homeostasis factors involved in dietary iron reduction, import and transport, that in part mimic those reported for the loss of hypoxic-induced transcription factor, HIF-2α. Our studies define a genetic basis for iron-deficiency anemia, a molecular approach for rescuing loss of nucleotidase function, and an unanticipated link between nucleotide hydrolysis in the sulfur assimilation pathway and iron homeostasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  8 / 8594 MEDLINE  
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[PMID]: 29455581
[Au] Autor:Resnik-Docampo M; Sauer V; Schinaman JM; Clark RI; Walker DW; Jones DL
[Ad] Address:a Department of Molecular , Cell, and Developmental Biology and University of California , Los Angeles , California , USA.
[Ti] Title:Keeping it tight: The relationship between bacterial dysbiosis, septate junctions, and the intestinal barrier in Drosophila.
[So] Source:Fly (Austin);:1-7, 2018 Mar 06.
[Is] ISSN:1933-6942
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Maladaptive changes in the intestinal flora, typically referred to as bacterial dysbiosis, have been linked to intestinal aging phenotypes, including an increase in intestinal stem cell (ISC) proliferation, activation of inflammatory pathways, and increased intestinal permeability . However, the causal relationships between these phenotypes are only beginning to be unravelled. We recently characterized the age-related changes that occur to septate junctions (SJ) between adjacent, absorptive enterocytes (EC) in the fly intestine. Changes could be observed in the overall level of SJ proteins, as well as the localization of a subset of SJ proteins. Such age-related changes were particularly noticeable at tricellular junctions (TCJ) . Acute loss of the Drosophila TCJ protein Gliotactin (Gli) in ECs led to rapid activation of stress signalling in stem cells and an increase in ISC proliferation, even under axenic conditions; a gradual disruption of the intestinal barrier was also observed. The uncoupling of changes in bacteria from alterations in ISC behaviour and loss of barrier integrity has allowed us to begin to explore the interrelationship of these intestinal aging phenotypes in more detail and has shed light on the importance of the proteins that contribute to maintenance of the intestinal barrier.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher
[do] DOI:10.1080/19336934.2018.1441651

  9 / 8594 MEDLINE  
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[PMID]: 29503179
[Au] Autor:Lee KA; Cho KC; Kim B; Jang IH; Nam K; Kwon YE; Kim M; Hyeon DY; Hwang D; Seol JH; Lee WJ
[Ad] Address:School of Biological Sciences, Seoul National University, Seoul 08826, South Korea; National Creative Research Initiative Center for Hologenomics, Seoul National University, Seoul 08826, South Korea; Institute of Molecular Biology and Genetics, Seoul National University, Seoul 151-742, South Korea.
[Ti] Title:Inflammation-Modulated Metabolic Reprogramming Is Required for DUOX-Dependent Gut Immunity in Drosophila.
[So] Source:Cell Host Microbe;, 2018 Feb 08.
[Is] ISSN:1934-6069
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:DUOX, a member of the NADPH oxidase family, acts as the first line of defense against enteric pathogens by producing microbicidal reactive oxygen species. DUOX is activated upon enteric infection, but the mechanisms regulating DUOX activity remain incompletely understood. Using Drosophila genetic tools, we show that enteric infection results in "pro-catabolic" signaling that initiates metabolic reprogramming of enterocytes toward lipid catabolism, which ultimately governs DUOX homeostasis. Infection induces signaling cascades involving TRAF3 and kinases AMPK and WTS, which regulate TOR kinase to control the balance of lipogenesis versus lipolysis. Enhancing lipogenesis blocks DUOX activity, whereas stimulating lipolysis via ATG1-dependent lipophagy is required for DUOX activation. Drosophila with altered activity in TRAF3-AMPK/WTS-ATG1 pathway components exhibit abolished infection-induced lipolysis, reduced DUOX activation, and enhanced susceptibility to enteric infection. Thus, this work uncovers signaling cascades governing inflammation-induced metabolic reprogramming and provides insight into the pathophysiology of immune-metabolic interactions in the microbe-laden gut epithelia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:Publisher

  10 / 8594 MEDLINE  
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[PMID]: 29476278
[Au] Autor:Ayehunie S; Landry T; Stevens Z; Armento A; Hayden P; Klausner M
[Ad] Address:MatTek Corporation, 200 Homer Avenue, Ashland, Massachusetts, USA. sayehunie@mattek.com.
[Ti] Title:Human Primary Cell-Based Organotypic Microtissues for Modeling Small Intestinal Drug Absorption.
[So] Source:Pharm Res;35(4):72, 2018 Feb 23.
[Is] ISSN:1573-904X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: The study evaluates the use of new in vitro primary human cell-based organotypic small intestinal (SMI) microtissues for predicting intestinal drug absorption and drug-drug interaction. METHODS: The SMI microtissues were reconstructed using human intestinal fibroblasts and enterocytes cultured on a permeable support. To evaluate the suitability of the intestinal microtissues to model drug absorption, the permeability coefficients across the microtissues were determined for a panel of 11 benchmark drugs with known human absorption and Caco-2 permeability data. Drug-drug interactions were examined using efflux transporter substrates and inhibitors. RESULTS: The 3D-intestinal microtissues recapitulate the structural features and physiological barrier properties of the human small intestine. The microtissues also expressed drug transporters and metabolizing enzymes found on the intestinal wall. Functionally, the SMI microtissues were able to discriminate between low and high permeability drugs and correlated better with human absorption data (r = 0.91) compared to Caco-2 cells (r = 0.71). Finally, the functionality of efflux transporters was confirmed using efflux substrates and inhibitors which resulted in efflux ratios of >2.0 fold and by a decrease in efflux ratios following the addition of inhibitors. CONCLUSION: The SMI microtissues appear to be a useful pre-clinical tool for predicting drug bioavailability of orally administered drugs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Data-Review
[do] DOI:10.1007/s11095-018-2362-0


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