PMID- 10792371
OWN - NLM
STAT- MEDLINE
DCOM- 20000627
LR  - 20190513
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 120
IP  - 2
DP  - 2000 May
TI  - Increased production of matrix metalloproteinase-3 and tissue inhibitor of 
      metalloproteinase-1 by inflamed mucosa in inflammatory bowel disease.
PG  - 241-6
AB  - Inflammatory bowel diseases (IBD) are characterized by a sustained inflammatory 
      cascade that gives rise to the release of mediators capable of degrading and 
      modifying bowel wall structure. Our aims were (i) to measure the production of 
      matrix metalloproteinase-3 (MMP-3), and its tissue inhibitor, tissue inhibitor of 
      metalloproteinase-1 (TIMP-1), by inflamed and uninflamed colonic mucosa in IBD, 
      and (ii) to correlate their production with that of proinflammatory cytokines and 
      the anti-inflammatory cytokine, IL-10. Thirty-eight patients with IBD, including 
      25 with Crohn's disease and 13 with ulcerative colitis, were included. Ten 
      controls were also studied. Biopsies were taken from inflamed and uninflamed 
      regions and inflammation was graded both macroscopically and histologically. 
      Organ cultures were performed for 18 h. Tumour necrosis factor-alpha (TNF-alpha), 
      IL-6, IL-1beta, IL-10, MMP-3 and TIMP-1 concentrations were measured using 
      specific immunoassays. The production of both MMP-3 and the TIMP-1 were either 
      undetectable or below the sensitivity of our immunoassay in the vast majority of 
      uninflamed samples either from controls or from those with Crohn's disease or 
      ulcerative colitis. In inflamed mucosa, the production of these mediators 
      increased significantly both in Crohn's disease (P < 0.01 and 0.001, 
      respectively) and ulcerative colitis (P < 0.001 and 0.001, respectively). 
      Mediator production in both cases was significantly correlated with the 
      production of proinflammatory cytokines and IL-10, as well as with the degree of 
      macroscopic and microscopic inflammation. Inflamed mucosa of both Crohn's disease 
      and ulcerative colitis show increased production of both MMP-3 and its tissue 
      inhibitor, which correlates very well with production of IL-1beta, IL-6, 
      TNF-alpha and IL-10.
FAU - Louis, E
AU  - Louis E
AD  - Department of Gastroenterology, Inflammatory Diseases Research Group, and 
      Department of Pathology, CHU, Liege, Belgium.
FAU - Ribbens, C
AU  - Ribbens C
FAU - Godon, A
AU  - Godon A
FAU - Franchimont, D
AU  - Franchimont D
FAU - De Groote, D
AU  - De Groote D
FAU - Hardy, N
AU  - Hardy N
FAU - Boniver, J
AU  - Boniver J
FAU - Belaiche, J
AU  - Belaiche J
FAU - Malaise, M
AU  - Malaise M
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 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Tissue Inhibitor of Metalloproteinase-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Adult
MH  - Colitis, Ulcerative/classification/immunology/*metabolism/pathology
MH  - Colon/pathology
MH  - Colonoscopy/methods
MH  - Crohn Disease/classification/immunology/*metabolism/pathology
MH  - Culture Techniques
MH  - Female
MH  - Humans
MH  - Interleukin-1/metabolism
MH  - Interleukin-10/metabolism
MH  - Interleukin-6/metabolism
MH  - Intestinal Mucosa/*metabolism
MH  - Male
MH  - Matrix Metalloproteinase 3/*biosynthesis
MH  - Middle Aged
MH  - Tissue Inhibitor of Metalloproteinase-1/*biosynthesis
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC1905637
EDAT- 2000/05/03 09:00
MHDA- 2000/07/06 11:00
PMCR- 2001/05/01
CRDT- 2000/05/03 09:00
PHST- 2000/05/03 09:00 [pubmed]
PHST- 2000/07/06 11:00 [medline]
PHST- 2000/05/03 09:00 [entrez]
PHST- 2001/05/01 00:00 [pmc-release]
AID - cei1227 [pii]
AID - 10.1046/j.1365-2249.2000.01227.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2000 May;120(2):241-6. doi: 10.1046/j.1365-2249.2000.01227.x.