title: Gene expression changes in the colon epithelium are similar to those of intact colon during late inflammation in interleukin-10 gene deficient mice.
abstract: In addition to their role in absorption and secretion, epithelial cells play an important role in the protection of the colon mucosa from the resident microbiota and are important for the maintenance of homeostasis. Microarray analysis of intact colon samples is widely used to gain an overview of the cellular pathways and processes that are active in the colon during inflammation. Laser microdissection of colon epithelial cells allows a more targeted analysis of molecular pathways in the mucosa, preceding and during inflammation, with potentially increased sensitivity to changes in specific cell populations. The aim of this study was to investigate the molecular changes that occur in early and late inflammation stages in colon epithelium of a mouse model of inflammatory bowel diseases. Microarray analysis of intact colon samples and microdissected colon epithelial cell samples from interleukin-10 gene deficient and control mice at 6 and 12 weeks of age was undertaken. Results of gene set enrichment analysis showed that more immune-related pathways were identified between interleukin-10 gene deficient and control mice at 6 weeks of age in epithelial cells than intact colon. This suggests that targeting epithelial cells could increase sensitivity for detecting immune changes that occur early in the inflammatory process. However, in the later stages of inflammation, microarray analyses of intact colon and epithelium both provide a similar overview of gene expression changes in the colon mucosa at the pathway level.
authors.affiliation: Food Nutrition & Health Team, Food & Bio-based Products Group, AgResearch Grasslands, Palmerston North, New Zealand.
authors.forename: Anna E
authors.initials: AE
authors.lastname: Russ
authors.forename: Jason S
authors.initials: JS
authors.lastname: Peters
authors.forename: Warren C
authors.initials: WC
authors.lastname: McNabb
authors.forename: Matthew P G
authors.initials: MP
authors.lastname: Barnett
authors.forename: Rachel C
authors.initials: RC
authors.lastname: Anderson
authors.forename: Zaneta
authors.initials: Z
authors.lastname: Park
authors.forename: Shuotun
authors.initials: S
authors.lastname: Zhu
authors.forename: Paul
authors.initials: P
authors.lastname: Maclean
authors.forename: Wayne
authors.initials: W
authors.lastname: Young
authors.forename: Gordon W
authors.initials: GW
authors.lastname: Reynolds
authors.forename: Nicole C
authors.initials: NC
authors.lastname: Roy
mesh_terms: D000818:Animals; D003106:Colon / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004847:Epithelial Cells / Q000276:immunology / Q000378:metabolism*; D053263:Gene Regulatory Networks; D018836:Inflammation Mediators / Q000378:metabolism; D015212:Inflammatory Bowel Diseases / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D016753:Interleukin-10 / Q000172:deficiency* / Q000235:genetics; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007421:Intestine, Small / Q000473:pathology; D061346:Laser Capture Microdissection; D051379:Mice; D057507:Mice, 129 Strain; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D020411:Oligonucleotide Array Sequence Analysis; D059467:Transcriptome
chemical_list: C556062:IL10 protein, mouse; D018836:Inflammation Mediators; D016753:Interleukin-10