title: Indoleamine 2,3-dioxygenase expression in human inflammatory bowel disease.
abstract: OBJECTIVE
  The study is carried out to identify the expression pattern of indoleamine 2,3-dioxygenase (IDO) in human Crohn's disease and ulcerative colitis and to investigate the effect of different therapies (salicylates, steroids, and antitumor necrosis factor antibody) on the intestinal expression of IDO.
  
  
  METHODS
  Immunohistochemistry was used. A total of 10 high power fields were counted for each patient.
  
  
  RESULTS
  IDO was expressed in the both lamina propria and epithelium. IDO expression increased in the lesions from ulcerative colitis and Crohn's disease and was positively related to the severity of inflammation. IDO-positive mononuclear cells also expressed CD11c, CD68, and TLR4. IDO expression decreased significantly after treatment with steroids and salicylates, but remained unchanged after infliximab therapy.
  
  
  CONCLUSIONS
  IDO was over-expressed in human inflammatory bowel disease. It may be a bridge between innate immunity and adaptive immunity. Steroids and salicylates may act through the inhibition of IDO expression. IDO upregulation may be a promising therapy to achieve inflammatory bowel disease remission.
authors.affiliation: Department of Gastroenterology, West China Hospital of Sichuan University, Chengdu, Sichuan, China.
authors.forename: Liping
authors.initials: L
authors.lastname: Zhou
authors.forename: Huan
authors.initials: H
authors.lastname: Chen
authors.forename: Quan
authors.initials: Q
authors.lastname: Wen
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D039521:CD11c Antigen / Q000378:metabolism; D003093:Colitis, Ulcerative / Q000188:drug therapy / Q000201:enzymology / Q000276:immunology; D003424:Crohn Disease / Q000188:drug therapy / Q000201:enzymology / Q000276:immunology; D004847:Epithelial Cells / Q000201:enzymology; D005260:Female; D005765:Gastrointestinal Agents / Q000627:therapeutic use; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007124:Immunoenzyme Techniques; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase / Q000378:metabolism*; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy / Q000201:enzymology* / Q000276:immunology; D000069285:Infliximab; D007413:Intestinal Mucosa / Q000201:enzymology; D008297:Male; D008875:Middle Aged; D012459:Salicylates / Q000627:therapeutic use; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D000097382:CD68 Molecule
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D039521:CD11c Antigen; D005765:Gastrointestinal Agents; D005938:Glucocorticoids; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase; D000069285:Infliximab; D012459:Salicylates; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C495345:TLR4 protein, human