Transcriptome profiling of the small intestinal epithelium in germfree versus conventional piglets
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Chowdhury, S. R., King, D. E., Willing, B. P., Band, M. R., Beever, J. E., Lane, A. B., Loor, J. J., Marini, J. C., Rund, L. A., Schook, L. B., Van Kessel, A. G., & Gaskins, H. R. (2007). Transcriptome profiling of the small intestinal epithelium in germfree versus conventional piglets. BMC Genomics, 8(215), [16 pages]. http://dx.doi.org/10.1186/1471-2164-8-215
Link to Related Item
http://dx.doi.org/10.1186/1471-2164-8-215
Abstract
Description
Background To gain insight into host-microbe interactions in a piglet model, a functional genomics approach was used to address the working hypothesis that transcriptionally regulated genes associated with promoting epithelial barrier function are activated as a defensive response to the intestinal microbiota. Cesarean-derived germfree (GF) newborn piglets were colonized with adult swine feces, and villus and crypt epithelial cell transcriptomes from colonized and GF neonatal piglets were compared using laser-capture microdissection and high-density porcine oligonucleotide microarray technology. Results Consistent with our hypothesis, resident microbiota induced the expression of genes contributing to intestinal epithelial cell turnover, mucus biosynthesis, and priming of the immune system. Furthermore, differential expression of genes associated with antigen presentation (pan SLA class I, B2M, TAP1 and TAPBP) demonstrated that microbiota induced immune responses using a distinct regulatory mechanism common for these genes. Specifically, gene network analysis revealed that microbial colonization activated both type I (IFNAR) and type II (IFNGR) interferon receptor mediated signaling cascades leading to enhanced expression of signal transducer and activator of transcription 1 (STAT1), STAT2 and IFN regulatory factor 7 (IRF7) transcription factors and the induction of IFN-inducible genes as a reflection of intestinal epithelial inflammation. In addition, activated RNA expression of NF-kappa-B inhibitor alpha (NFκBIA; a.k.a I-kappa-B-alpha, IKBα) and toll interacting protein (TOLLIP), both inhibitors of inflammation, along with downregulated expression of the immunoregulatory transcription factor GATA binding protein-1 (GATA1) is consistent with the maintenance of intestinal homeostasis. Conclusion This study supports the concept that the intestinal epithelium has evolved to maintain a physiological state of inflammation with respect to continuous microbial exposure, which serves to sustain a tight intestinal barrier while preventing overt inflammatory responses that would compromise barrier function.
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http://purl.org/coar/resource_type/c_6501 http://purl.org/coar/version/c_970fb48d4fbd8a85
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Attribution 4.0 International
Subject/Keywords
Host-Parasite Interactions/Genetics
Signal Transduction/Genetics
Gene Regulatory Networks
Germ-Free Life/Genetics
Animals, Newborn
Intestine, Small/Metabolism
Intestinal Mucosa/Cytology
Principal components analysis
Intestinal Mucosa/Immunology
Metabolic Networks And Pathways/Genetics
Oligonucleotide Array Sequence Analysis
Immunity, Mucosal/Genetics
Cell Proliferation
Electron Transport/Genetics
Intestine, Small/Microbiology
Intestine, Small/Immunology
Gene Expression Profiling
Intestinal Mucosa/Metabolism
Cell Differentiation/Genetics
Transcription, Genetic
Swine
Animals
Intestinal Mucosa/Microbiology
Signal Transduction/Genetics
Gene Regulatory Networks
Germ-Free Life/Genetics
Animals, Newborn
Intestine, Small/Metabolism
Intestinal Mucosa/Cytology
Principal components analysis
Intestinal Mucosa/Immunology
Metabolic Networks And Pathways/Genetics
Oligonucleotide Array Sequence Analysis
Immunity, Mucosal/Genetics
Cell Proliferation
Electron Transport/Genetics
Intestine, Small/Microbiology
Intestine, Small/Immunology
Gene Expression Profiling
Intestinal Mucosa/Metabolism
Cell Differentiation/Genetics
Transcription, Genetic
Swine
Animals
Intestinal Mucosa/Microbiology
Language
en