PMID- 23600829
OWN - NLM
STAT- MEDLINE
DCOM- 20130624
LR  - 20211021
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 172
IP  - 3
DP  - 2013 Jun
TI  - Epithelial expression of interleukin-37b in inflammatory bowel disease.
PG  - 410-6
LID - 10.1111/cei.12061 [doi]
AB  - Interleukin (IL)-37 is a member of the IL-1 cytokine family. We investigated 
      IL-37b expression in the inflamed mucosa of inflammatory bowel disease (IBD) 
      patients. Furthermore, we analysed IL-37b expression in human colonic epithelial 
      cells. The human colonic epithelial cell line T84 and human colonic subepithelial 
      myofibroblasts (SEMFs) were used. IL-37b expression in the IBD mucosa was 
      evaluated by immunohistochemistry. IL-37b mRNA and protein expression were 
      determined by real time-polymerase chain reaction (PCR) and Western blotting, 
      respectively. IL-37b was not detected in the normal colonic mucosa. In the 
      inflamed mucosa of IBD patients, epithelial IL-37b expression was increased 
      markedly. In ulcerative colitis (UC) and Crohn's disease (CD) patients, IL-37b 
      expression was enhanced in the affected mucosa. In the intestinal epithelial cell 
      line T84, the expression of IL-37b mRNA and protein was enhanced by tumour 
      necrosis factor (TNF)-alpha. This IL-37b induction by TNF-alpha was mediated by nuclear 
      factor (NF)-kappaB and activator protein (AP)-1 activation. Furthermore, IL-37b 
      inhibited TNF-alpha-induced interferon-gamma-inducible protein (IP)-10 expression 
      significantly in human colonic SEMFs. Epithelial IL-37b expression was increased 
      in IBD patients, especially UC patients. IL-37b may be involved in the 
      pathophysiology of IBD as an anti-inflammatory cytokine and an inhibitor of both 
      innate and acquired immune responses.
CI  - (c) 2013 British Society for Immunology.
FAU - Imaeda, H
AU  - Imaeda H
AD  - Department of Medicine, Shiga University of Medical Science, Otsu, Japan.
FAU - Takahashi, K
AU  - Takahashi K
FAU - Fujimoto, T
AU  - Fujimoto T
FAU - Kasumi, E
AU  - Kasumi E
FAU - Ban, H
AU  - Ban H
FAU - Bamba, S
AU  - Bamba S
FAU - Sonoda, H
AU  - Sonoda H
FAU - Shimizu, T
AU  - Shimizu T
FAU - Fujiyama, Y
AU  - Fujiyama Y
FAU - Andoh, A
AU  - Andoh A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (CXCL10 protein, human)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (IL37 protein, human)
RN  - 0 (Interleukin-1)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
SB  - IM
MH  - Adaptive Immunity
MH  - Caco-2 Cells
MH  - Case-Control Studies
MH  - Cells, Cultured
MH  - Chemokine CXCL10/genetics/metabolism
MH  - Colitis, Ulcerative/genetics/immunology/metabolism/pathology
MH  - Crohn Disease/genetics/immunology/metabolism/pathology
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Immunity, Innate
MH  - Inflammatory Bowel Diseases/genetics/*immunology/metabolism/pathology
MH  - Interleukin-1/genetics/*metabolism
MH  - Intestinal Mucosa/drug effects/immunology/metabolism/pathology
MH  - MAP Kinase Signaling System
MH  - Myofibroblasts/drug effects/immunology/metabolism/pathology
MH  - NF-kappa B/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Transcription Factor AP-1/metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
PMC - PMC3646440
EDAT- 2013/04/23 06:00
MHDA- 2013/06/26 06:00
PMCR- 2014/06/01
CRDT- 2013/04/23 06:00
PHST- 2012/12/17 00:00 [accepted]
PHST- 2013/04/23 06:00 [entrez]
PHST- 2013/04/23 06:00 [pubmed]
PHST- 2013/06/26 06:00 [medline]
PHST- 2014/06/01 00:00 [pmc-release]
AID - 10.1111/cei.12061 [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2013 Jun;172(3):410-6. doi: 10.1111/cei.12061.