PMID- 17879274
OWN - NLM
STAT- MEDLINE
DCOM- 20080221
LR  - 20220409
IS  - 1078-0998 (Print)
IS  - 1078-0998 (Linking)
VI  - 14
IP  - 1
DP  - 2008 Jan
TI  - Local and systemic interleukin-18 and interleukin-18-binding protein in children 
      with inflammatory bowel disease.
PG  - 68-74
AB  - BACKGROUND: Interleukin-18 (IL-18) is increased in the inflamed mucosa of 
      patients with Crohn's disease (CD). The balance between this pleiotropic 
      proinflammatory cytokine and its natural inhibitor, IL-18-binding protein 
      (IL-18BP), may contribute to the pathogenesis of inflammatory bowel disease 
      (IBD). METHODS: Serum and mucosal biopsies were collected from children with IBD, 
      from children with celiac disease, and from controls. Biopsies were maintained in 
      culture for 24 hours, and supernatant was collected. Serum and supernatant IL-18 
      and IL-18BPa concentrations were measured by immunoassay. Disease activity score 
      (PCDAI) and standard serum inflammatory markers (albumin, platelets, ESR, and 
      CRP) were recorded. RESULTS: Serum IL-18 was greater in children with CD (537 
      pg/mL) than in controls (335 pg/mL; P < 0.05) but not in children with ulcerative 
      colitis (UC) or IBD type unclassified (IBDU). Mucosal IL-18 was greater in 
      children with CD and UC/IBDU than in controls (P < 0.01). Serum IL-18BPa was 
      increased in children with CD compared with that in controls (3.9 versus 2.6 
      ng/mL; P < 0.05), but was not elevated in children with UC/IBDU. Furthermore, 
      calculated free-serum IL-18 was elevated in CD, but not UC/IBDU, compared with 
      that in controls (P = 0.001). Total and free-serum IL-18 were elevated in severe 
      CD relative to in mild/moderate disease. CONCLUSIONS: IL-18, produced in the 
      colons of children with IBD, may contribute to local inflammatory changes. 
      Systemic IL-18 level may be a useful indicator of gut inflammation. Furthermore, 
      free IL-18 is greatly elevated in children with CD, suggesting that compensatory 
      increases in IL-18BPa are insufficient. Further exploration of the role of this 
      cytokine in the pathogenesis of IBD is now required.
FAU - Leach, Steven T
AU  - Leach ST
AD  - School of Women's and Children's Health, University of New South Wales, 
      Australia.
FAU - Messina, Isabella
AU  - Messina I
FAU - Lemberg, Daniel A
AU  - Lemberg DA
FAU - Novick, Daniela
AU  - Novick D
FAU - Rubenstein, Menachem
AU  - Rubenstein M
FAU - Day, Andrew S
AU  - Day AS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Inflamm Bowel Dis
JT  - Inflammatory bowel diseases
JID - 9508162
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interleukin-18)
RN  - 0 (interleukin-18 binding protein)
SB  - IM
MH  - Adolescent
MH  - Biopsy
MH  - Blood Chemical Analysis
MH  - Celiac Disease/immunology
MH  - Child
MH  - Child, Preschool
MH  - Colitis, Ulcerative/*immunology
MH  - Crohn Disease/*immunology
MH  - Female
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/*analysis/blood
MH  - Interleukin-18/*analysis/blood
MH  - Intestinal Mucosa/*chemistry
MH  - Male
MH  - Severity of Illness Index
EDAT- 2007/09/20 09:00
MHDA- 2008/02/22 09:00
CRDT- 2007/09/20 09:00
PHST- 2007/09/20 09:00 [pubmed]
PHST- 2008/02/22 09:00 [medline]
PHST- 2007/09/20 09:00 [entrez]
AID - 10.1002/ibd.20272 [doi]
PST - ppublish
SO  - Inflamm Bowel Dis. 2008 Jan;14(1):68-74. doi: 10.1002/ibd.20272.