PMID- 22141367
OWN - NLM
STAT- MEDLINE
DCOM- 20120921
LR  - 20171116
IS  - 1440-1746 (Electronic)
IS  - 0815-9319 (Linking)
VI  - 27
IP  - 5
DP  - 2012 May
TI  - Characteristics of intestinal lamina propria dendritic cells in a mouse model of 
      postinfectious irritable bowel syndrome.
PG  - 935-44
LID - 10.1111/j.1440-1746.2011.07046.x [doi]
AB  - BACKGROUND AND AIM: 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.
CI  - (c) 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell 
      Publishing Asia Pty Ltd.
FAU - Long, Yanqin
AU  - Long Y
AD  - Division of Gastroenterology, Union Hospital of Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, China.
FAU - Wang, Wenfeng
AU  - Wang W
FAU - Wang, Huan
AU  - Wang H
FAU - Hao, Liangcheng
AU  - Hao L
FAU - Qian, Wei
AU  - Qian W
FAU - Hou, Xiaohua
AU  - Hou X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - J Gastroenterol Hepatol
JT  - Journal of gastroenterology and hepatology
JID - 8607909
RN  - 0 (B7-2 Antigen)
RN  - 0 (Cytokines)
RN  - 0 (Histocompatibility Antigens Class II)
SB  - IM
CIN - J Gastroenterol Hepatol. 2012 May;27(5):847-8. PMID: 22515804
MH  - Animals
MH  - B7-2 Antigen/metabolism
MH  - CD4-Positive T-Lymphocytes/physiology
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Chemotaxis
MH  - Cytokines/*metabolism
MH  - Dendritic Cells/*immunology/metabolism
MH  - Histocompatibility Antigens Class II/metabolism
MH  - Hyperalgesia/etiology
MH  - Intestinal Mucosa
MH  - Irritable Bowel Syndrome/*immunology
MH  - Lymphocyte Culture Test, Mixed
MH  - Mice
MH  - Models, Animal
MH  - Phenotype
MH  - Reflex, Abdominal
MH  - *Trichinella spiralis
MH  - Trichinellosis/complications/*immunology/pathology
EDAT- 2011/12/07 06:00
MHDA- 2012/09/22 06:00
CRDT- 2011/12/07 06:00
PHST- 2011/12/07 06:00 [entrez]
PHST- 2011/12/07 06:00 [pubmed]
PHST- 2012/09/22 06:00 [medline]
AID - 10.1111/j.1440-1746.2011.07046.x [doi]
PST - ppublish
SO  - J Gastroenterol Hepatol. 2012 May;27(5):935-44. doi: 
      10.1111/j.1440-1746.2011.07046.x.