title: Transcriptome signatures in Helicobacter pylori-infected mucosa identifies acidic mammalian chitinase loss as a corpus atrophy marker.
abstract: BACKGROUND
  The majority of gastric cancer cases are believed to be caused by chronic infection with the bacterium Helicobacter pylori, and atrophic corpus gastritis is a predisposing condition to gastric cancer development. We aimed to increase understanding of the molecular details of atrophy by performing a global transcriptome analysis of stomach tissue.
  
  
  METHODS
  Biopsies from patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa and analyzed on microarrays. The stages included patients without current H. pylori infection, H. pylori-infected without corpus atrophy and patients with current or past H. pylori-infection with corpus-predominant atrophic gastritis.
  
  
  RESULTS
  Using clustering and integrated analysis, we found firm evidence for antralization of the corpus mucosa of atrophy patients. This antralization harbored gain of gastrin expression, as well as loss of expression of corpus-related genes, such as genes associated with acid production, energy metabolism and blood clotting. The analyses provided detailed molecular evidence for simultaneous intestinal metaplasia (IM) and spasmolytic polypeptide expressing metaplasia (SPEM) in atrophic corpus tissue. Finally, acidic mammalian chitinase, a chitin-degrading enzyme produced by chief cells, was shown to be strongly down-regulated in corpus atrophy.
  
  
  CONCLUSIONS
  Transcriptome analysis revealed several gene groups which are related to development of corpus atrophy, some of which were increased also in H. pylori-infected non-atrophic patients. Furthermore, loss of acidic chitinase expression is a promising marker for corpus atrophy.
authors.affiliation: Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. samuel.lundin@gu.se.
authors.forename: Intawat
authors.initials: I
authors.lastname: Nookaew
authors.forename: Kaisa
authors.initials: K
authors.lastname: Thorell
authors.forename: Kuntal
authors.initials: K
authors.lastname: Worah
authors.forename: Shugui
authors.initials: S
authors.lastname: Wang
authors.forename: Martin Lloyd
authors.initials: ML
authors.lastname: Hibberd
authors.forename: Henrik
authors.initials: H
authors.lastname: Sjövall
authors.forename: Sven
authors.initials: S
authors.lastname: Pettersson
authors.forename: Jens
authors.initials: J
authors.lastname: Nielsen
authors.forename: Samuel B
authors.initials: SB
authors.lastname: Lundin
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000378:metabolism; D001808:Blood Vessels / Q000503:physiopathology; D002688:Chitinases / Q000172:deficiency / Q000235:genetics*; D004734:Energy Metabolism / Q000235:genetics; D005260:Female; D005753:Gastric Mucosa / Q000098:blood supply / Q000378:metabolism / Q000382:microbiology*; D005757:Gastritis, Atrophic / Q000201:enzymology* / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis; D014158:Transcription, Genetic; D059467:Transcriptome
chemical_list: D015415:Biomarkers; C499254:CHIA protein, human; D002688:Chitinases