title: Cholera toxin suppresses expression of ubiquitin editing enzyme A20 and enhances transcytosis.
abstract: BACKGROUND
  The ubiquitin editing enzyme A20 plays an important role in maintaining the homeostasis in the body Microbe-derived adjuvants are commonly used in animal models of intestinal allergy.
  
  
  OBJECTIVE
  This study aims to investigate the role of cholera toxin-induced A20 suppression in compromising intestinal barrier function.
  
  
  METHODS
  Human intestinal epithelial cells were cultured into monolayers as an in vitro epithelial barrier model. Ovalbumin (OVA) was used as a specific allergen to test the degrading capability of intestinal epithelial cells for the endocytic allergens. The fusion of endosomes and lysosomes in epithelial cells was observed by immunocytochemistry. The antigenicity of OVA was tested by T cell proliferation assay.
  
  
  RESULTS
  A20 was detectable in the intestinal cell lines and mouse intestinal epithelialum. A20 was required in the degradation of endocytic allergens in HT-29 cells. The allergen, OVA, could pass through A20-deficient HT-29 monolayer barrier. Exposure to microbial adjuvant, cholera toxin, suppressed the expression of A20 in HT-29 cells, which compromised the epithelial barrier function.
  
  
  CONCLUSIONS
  The microbial product, cholera toxin, interferes with the expression of A20 in intestinal epithelial cells, which compromises the intestinal epithelial barrier function.
authors.affiliation: Department of Digestive Endoscopy, Division of South Building, Chinese People's Liberation Army General Hospital, Beijing, China.
authors.forename: Ming-Yang
authors.initials: MY
authors.lastname: Li
authors.forename: Min
authors.initials: M
authors.lastname: Zhu
authors.forename: Bing
authors.initials: B
authors.lastname: Zhu
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Wang
mesh_terms: D000818:Animals; D018938:Caco-2 Cells; D002460:Cell Line; D002772:Cholera Toxin / Q000494:pharmacology*; D004268:DNA-Binding Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D011992:Endosomes / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D019073:HT29 Cells; D006801:Humans; D007150:Immunohistochemistry; D047908:Intracellular Signaling Peptides and Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D008247:Lysosomes / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D009687:Nuclear Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D010047:Ovalbumin / Q000276:immunology / Q000378:metabolism; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000378:metabolism; D057900:Transcytosis / Q000187:drug effects*; D000072598:Tumor Necrosis Factor alpha-Induced Protein 3
chemical_list: D004268:DNA-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; D009687:Nuclear Proteins; D034741:RNA, Small Interfering; D010047:Ovalbumin; D002772:Cholera Toxin; C076529:TNFAIP3 protein, human; D000072598:Tumor Necrosis Factor alpha-Induced Protein 3