title: Characteristics of intestinal lamina propria dendritic cells in a mouse model of postinfectious irritable bowel syndrome.
abstract: OBJECTIVE
  Postinfectious irritable bowel syndrome (PI-IBS), which results from inflammation has been emphasized a lot recently. Dendritic cells (DCs) may contribute to intestinal mucosal immune activation in the pathogenesis of PI-IBS. This study tested the hypothesis that phenotype and function of intestinal lamina propria DCs (LPDCs) changed in the development of a PI-IBS mouse model.
  
  
  METHODS
  Mice infected with Trichinella spiralis underwent abdominal withdrawal reflex (AWR) to evaluate visceral sensitivity. LPDCs were isolated and purified by intestine digestion and magnetic label-based technique. Surface markers were analyzed by flow cytometry. Endocytic activity, mixed lymphocyte reaction (MLR) and chemotaxis were studied. Cytokine production of the LPDCs cocultured with CD4(+) T cells was determined.
  
  
  RESULTS
  Intestinal inflammation resolved after 8 weeks infection with sustained visceral hyperalgesia. Surface markers CD86 and MHCII were lower in the acute infection group, but increased in the PI-IBS stage. Enhanced ability of endocytic activity and decreased abilities to attract and stimulate CD4(+) T cell proliferation were in the acute infection group. However, LPDCs in the PI-IBS stage showed weakened endocytic ability with enhanced abilities to attract and stimulate CD4(+) T cell proliferation. Cocultured LPDCs with CD4(+) T cells showed a predominant Th2 response in the acute infection stage, and more important roles of Th1, Th17 responses in the PI-IBS stage.
  
  
  CONCLUSIONS
  The hypothesis was supported that the phenotype and function of LPDCs changed in the development of PI-IBS, which induced the maintenance of intestinal mucosal immune activation and might provide a clue for the treatment of the disease.
authors.affiliation: Division of Gastroenterology, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Yanqin
authors.initials: Y
authors.lastname: Long
authors.forename: Wenfeng
authors.initials: W
authors.lastname: Wang
authors.forename: Huan
authors.initials: H
authors.lastname: Wang
authors.forename: Liangcheng
authors.initials: L
authors.lastname: Hao
authors.forename: Wei
authors.initials: W
authors.lastname: Qian
authors.forename: Xiaohua
authors.initials: X
authors.lastname: Hou
mesh_terms: D000818:Animals; D051940:B7-2 Antigen / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology; D049109:Cell Proliferation; D002478:Cells, Cultured; D002633:Chemotaxis; D016207:Cytokines / Q000378:metabolism*; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D006930:Hyperalgesia / Q000209:etiology; D007413:Intestinal Mucosa; D043183:Irritable Bowel Syndrome / Q000276:immunology*; D007959:Lymphocyte Culture Test, Mixed; D051379:Mice; D023421:Models, Animal; D010641:Phenotype; D012020:Reflex, Abdominal; D017160:Trichinella spiralis; D014235:Trichinellosis / Q000150:complications / Q000276:immunology* / Q000473:pathology
chemical_list: D051940:B7-2 Antigen; D016207:Cytokines; D000949:Histocompatibility Antigens Class II