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Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus

Germ-free piglets were orally infected with virulent rotavirus to collect jejunal mucosal scrapings at 12 and 18 hours post infection (two piglets per time point). IFN-gamma mRNA expression was stimulated in the mucosa of all four infected piglets, indicating that they all responded to the rotavirus...

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Autores principales: Hulst, Marcel, Kerstens, Hinri, de Wit, Agnes, Smits, Mari, van der Meulen, Jan, Niewold, Theo
Formato: Texto
Lenguaje:English
Publicado: Springer Vienna 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2441536/
https://www.ncbi.nlm.nih.gov/pubmed/18523839
http://dx.doi.org/10.1007/s00705-008-0118-6
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author Hulst, Marcel
Kerstens, Hinri
de Wit, Agnes
Smits, Mari
van der Meulen, Jan
Niewold, Theo
author_facet Hulst, Marcel
Kerstens, Hinri
de Wit, Agnes
Smits, Mari
van der Meulen, Jan
Niewold, Theo
author_sort Hulst, Marcel
collection PubMed
description Germ-free piglets were orally infected with virulent rotavirus to collect jejunal mucosal scrapings at 12 and 18 hours post infection (two piglets per time point). IFN-gamma mRNA expression was stimulated in the mucosa of all four infected piglets, indicating that they all responded to the rotavirus infection. RNA pools prepared from two infected piglets were used to compare whole mucosal gene expression at 12 and 18 hpi to expression in uninfected germ-free piglets (n = 3) using a porcine intestinal cDNA microarray. Microarray analysis identified 13 down-regulated and 17 up-regulated genes. Northern blot analysis of a selected group of genes confirmed the data of the microarray. Genes were functionally clustered in interferon-regulated genes, proliferation/differentiation genes, apoptosis genes, cytoskeleton genes, signal transduction genes, and enterocyte digestive, absorptive, and transport genes. Down-regulation of the transport gene cluster reflected in part the loss of rotavirus-infected enterocytes from the villous tips. Data mining suggested that several genes were regulated in lower- or mid-villus immature enterocytes and goblet cells, probably to support repair of the damaged epithelial cell layer at the villous tips. Furthermore, up-regulation was observed for IFN-γ induced guanylate binding protein 2, a protein that effectively inhibited VSV and EMCV replication in vitro (Arch Virol 150:1213–1220, 2005). This protein may play a role in the small intestine’s innate defense against enteric viruses like rotavirus. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00705-008-0118-6) contains supplementary material, which is available to authorized users.
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spelling pubmed-24415362008-06-27 Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus Hulst, Marcel Kerstens, Hinri de Wit, Agnes Smits, Mari van der Meulen, Jan Niewold, Theo Arch Virol Original Article Germ-free piglets were orally infected with virulent rotavirus to collect jejunal mucosal scrapings at 12 and 18 hours post infection (two piglets per time point). IFN-gamma mRNA expression was stimulated in the mucosa of all four infected piglets, indicating that they all responded to the rotavirus infection. RNA pools prepared from two infected piglets were used to compare whole mucosal gene expression at 12 and 18 hpi to expression in uninfected germ-free piglets (n = 3) using a porcine intestinal cDNA microarray. Microarray analysis identified 13 down-regulated and 17 up-regulated genes. Northern blot analysis of a selected group of genes confirmed the data of the microarray. Genes were functionally clustered in interferon-regulated genes, proliferation/differentiation genes, apoptosis genes, cytoskeleton genes, signal transduction genes, and enterocyte digestive, absorptive, and transport genes. Down-regulation of the transport gene cluster reflected in part the loss of rotavirus-infected enterocytes from the villous tips. Data mining suggested that several genes were regulated in lower- or mid-villus immature enterocytes and goblet cells, probably to support repair of the damaged epithelial cell layer at the villous tips. Furthermore, up-regulation was observed for IFN-γ induced guanylate binding protein 2, a protein that effectively inhibited VSV and EMCV replication in vitro (Arch Virol 150:1213–1220, 2005). This protein may play a role in the small intestine’s innate defense against enteric viruses like rotavirus. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00705-008-0118-6) contains supplementary material, which is available to authorized users. Springer Vienna 2008-06-04 2008 /pmc/articles/PMC2441536/ /pubmed/18523839 http://dx.doi.org/10.1007/s00705-008-0118-6 Text en © The Author(s) 2008 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Original Article
Hulst, Marcel
Kerstens, Hinri
de Wit, Agnes
Smits, Mari
van der Meulen, Jan
Niewold, Theo
Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus
title Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus
title_full Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus
title_fullStr Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus
title_full_unstemmed Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus
title_short Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus
title_sort early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2441536/
https://www.ncbi.nlm.nih.gov/pubmed/18523839
http://dx.doi.org/10.1007/s00705-008-0118-6
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