title: Induction of microRNA-155 during Helicobacter pylori infection and its negative regulatory role in the inflammatory response.
abstract: BACKGROUND
  MicroRNAs (miRNAs) are small, noncoding RNAs that regulate gene expression at posttranscriptional level. H. pylori is a major human pathogenic bacterium in gastric mucosa. To date, the role of miRNAs in response to H. pylori infection has not been explored.
  
  
  METHODS
  The expression profile of cellular miRNAs during H. pylori infection was analyzed by using microarray and quantitative reverse-transcriptase polymerase chain reaction. The potential target of miR-155 was identified by luciferase assay and Western blot. Promoter analysis and inhibitor experiment were used to investigate the pathway involved in the induction of miR-155. Examination of miR-155 function was performed by overexpression and inhibition of miR-155.
  
  
  RESULTS
  H. pylori was able to increase the miR-155 expression in gastric epithelial cell lines and gastric mucosal tissues, and nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) pathway were required for the induction of miR-155. miR-155 may down-regulate IkappaB kinase epsilon, Sma- and Mad-related protein 2 (SMAD2), and Fas-associated death domain protein. Furthermore, the overexpression of miR-155 negatively regulated the release of interleukin-8 and growth-related oncogene-alpha.
  
  
  CONCLUSIONS
  This study provides the first description of increased expression of miR-155 in H. pylori infection, and miR-155 may function as novel negative regulator that help to fine-tune the inflammation response of H. pylori infection.
authors: Department of Clinical Microbiology and Immunology, College of Medical Laboratory Science, Southwest Hospital, Third Military Medical University, No. 30 Gaotanyan Street, Chongqing, China.
authors: Bin
authors: B
authors: Xiao
authors: Zhen
authors: Z
authors: Liu
authors: Bo-Sheng
authors: BS
authors: Li
authors: Bin
authors: B
authors: Tang
authors: Wei
authors: W
authors: Li
authors: Gang
authors: G
authors: Guo
authors: Yun
authors: Y
authors: Shi
authors: Fengjun
authors: F
authors: Wang
authors: Yuan
authors: Y
authors: Wu
authors: Wen-De
authors: WD
authors: Tong
authors: Hong
authors: H
authors: Guo
authors: Xu-Hu
authors: XH
authors: Mao
authors: Quan-Ming
authors: QM
authors: Zou
mesh_terms: D000328:Adult; D054360:Chemokine CXCL1 / Q000378:metabolism; D053200:Fas-Associated Death Domain Protein / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D016481:Helicobacter Infections / Q000378:metabolism / Q000382:microbiology*; D016480:Helicobacter pylori; D006801:Humans; D051550:I-kappa B Kinase / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism*; D016209:Interleukin-8 / Q000378:metabolism; D008297:Male; D035683:MicroRNAs / Q000378:metabolism*; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D051899:Smad2 Protein / Q000378:metabolism
chemical_list: C475829:CXCL1 protein, human; D054360:Chemokine CXCL1; C505533:FADD protein, human; D053200:Fas-Associated Death Domain Protein; D016209:Interleukin-8; C524942:MIRN155 microRNA, human; D035683:MicroRNAs; D016328:NF-kappa B; C497782:SMAD2 protein, human; D051899:Smad2 Protein; D051550:I-kappa B Kinase