title: Site-specific programming of the host epithelial transcriptome by the gut microbiota.
abstract: BACKGROUND
  The intestinal epithelium separates us from the microbiota but also interacts with it and thus affects host immune status and physiology. Previous studies investigated microbiota-induced responses in the gut using intact tissues or unfractionated epithelial cells, thereby limiting conclusions about regional differences in the epithelium. Here, we sought to investigate microbiota-induced transcriptional responses in specific fractions of intestinal epithelial cells. To this end, we used microarray analysis of laser capture microdissection (LCM)-harvested ileal and colonic tip and crypt epithelial fractions from germ-free and conventionally raised mice and from mice during the time course of colonization.
  
  
  RESULTS
  We found that about 10% of the host's transcriptome was microbially regulated, mainly including genes annotated with functions in immunity, cell proliferation, and metabolism. The microbial impact on host gene expression was highly site specific, as epithelial responses to the microbiota differed between cell fractions. Specific transcriptional regulators were enriched in each fraction. In general, the gut microbiota induced a more rapid response in the colon than in the ileum.
  
  
  CONCLUSIONS
  Our study indicates that the microbiota engage different regulatory networks to alter host gene expression in a particular niche. Understanding host-microbiota interactions on a cellular level may facilitate signaling pathways that contribute to health and disease and thus provide new therapeutic strategies.
authors.affiliation: The Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, 41345, Sweden. Felix.Sommer@wlab.gu.se.
authors.forename: Felix
authors.initials: F
authors.lastname: Sommer
authors.affiliation: Department of Chemical and Biological Engineering, Chalmers University of Technology, Gothenburg, 41296, Sweden. intawat@chalmers.se.|Present Address: Comparative Genomics Group, Biosciences Division, Oak Ridge National Laboratory, Oak Ridge, TN, 37831, USA. intawat@chalmers.se.
authors.forename: Intawat
authors.initials: I
authors.lastname: Nookaew
authors.affiliation: The Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, 41345, Sweden. Nina.Sommer@wlab.gu.se.
authors.forename: Nina
authors.initials: N
authors.lastname: Sommer
authors.affiliation: The Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, 41345, Sweden. Per.Fogelstrand@wlab.gu.se.
authors.forename: Per
authors.initials: P
authors.lastname: Fogelstrand
authors.affiliation: The Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, 41345, Sweden. fredrik.backhed@wlab.gu.se.|Novo Nordisk Foundation Center for Basic Metabolic Research, Section for Metabolic Receptology and Enteroendocrinology, Faculty of Health Sciences, University of Copenhagen, Copenhagen, DK-2200, Denmark. fredrik.backhed@wlab.gu.se.
authors.forename: Fredrik
authors.initials: F
authors.lastname: Bäckhed
mesh_terms: D000818:Animals; D004847:Epithelial Cells / Q000276:immunology / Q000378:metabolism*; D000069196:Gastrointestinal Microbiome / Q000235:genetics* / Q000276:immunology; D041981:Gastrointestinal Tract / Q000276:immunology / Q000382:microbiology; D005786:Gene Expression Regulation; D007107:Immune System; D051379:Mice; D046228:Microarray Analysis; D064307:Microbiota / Q000276:immunology; D015398:Signal Transduction; D059467:Transcriptome