PMID- 19225717
OWN - NLM
STAT- MEDLINE
DCOM- 20091009
LR  - 20220409
IS  - 1591-9528 (Electronic)
IS  - 1591-8890 (Linking)
VI  - 9
IP  - 3
DP  - 2009 Sep
TI  - Expression of interleukin-18, IL-18BP, and IL-18R in serum, synovial fluid, and 
      synovial tissue in patients with rheumatoid arthritis.
PG  - 215-21
LID - 10.1007/s10238-009-0036-2 [doi]
AB  - Rheumatoid arthritis (RA) is a chronic immunological disease, the invasive 
      monocytes/macrophages and lymphocytes present in synovial cells and synovial 
      tissue produce many cytokines and inflammatory mediators by paracrine signaling 
      and plays a role in the pathological progress in RA patients. Interleukin-18 
      (IL-18) is a representative proinflammatory factor and displays multiple 
      biological functions. This study was designed to investigate the expression of 
      IL-18 and its receptor (IL-18R) and IL-18 binding protein (IL-18BP) in serum, 
      synovial fluid, and synovial tissue of patients with RA, and to identify the 
      pathological role of IL-18 in RA. Serum, synovial fluid, and synovial tissue were 
      obtained from RA patients. Samples from patients with osteoarthritis and healthy 
      people were obtained as controls. Levels of IL-18, IL-18BP, and PGE2 in serum and 
      synovial fluid were measured by enzyme-linked immunosorbent assay. The biological 
      activity of IL-18 in serum and synovial fluid was detected on the basis of 
      IFN-gamma secretion from IL-18-responding human myelomonocytic KG-1 cells. NO in 
      serum and synovial fluid was detected by Griess reaction. Expression of IL-18, 
      IL-18BP, IL-18R, iNOS, and COX-2 mRNA and protein in synovial tissues was 
      determined by quantitative reverse transcriptase polymerase chain reaction and 
      Western blot. This study shows the expression levels of IL-18, IL-18R, iNOS, 
      COX-2, and the biological activity of IL-18 in both serum and synovial fluid and 
      tissue of patients with RA were significantly increased compared with the 
      corresponding samples from the two control groups. In addition, expression of 
      IL-18BP in patients with RA was decreased compared with samples from the two 
      control groups. In conclusion, the overexpression of IL-18 and IL-18R may play an 
      important role in the pathogenesis of RA.
FAU - Shao, Xue-Ting
AU  - Shao XT
AD  - State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, 
      Institute of Infectious Diseases, The First Affiliated Hospital, Zhejiang 
      University School of Medicine, Hangzhou 310003, China.
FAU - Feng, Lei
AU  - Feng L
FAU - Gu, Li-Juan
AU  - Gu LJ
FAU - Wu, Li-Juan
AU  - Wu LJ
FAU - Feng, Ting-Ting
AU  - Feng TT
FAU - Yang, Yun-Mei
AU  - Yang YM
FAU - Wu, Nan-Ping
AU  - Wu NP
FAU - Yao, Hang-Ping
AU  - Yao HP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090219
PL  - Italy
TA  - Clin Exp Med
JT  - Clinical and experimental medicine
JID - 100973405
RN  - 0 (IL18R1 protein, human)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interleukin-18)
RN  - 0 (Interleukin-18 Receptor alpha Subunit)
RN  - 0 (interleukin-18 binding protein)
RN  - 82115-62-6 (Interferon-gamma)
RN  - EC 1.14.13.39 (NOS2 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (PTGS2 protein, human)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Arthritis, Rheumatoid/*immunology/pathology
MH  - Blotting, Western
MH  - Cell Line
MH  - Cyclooxygenase 2/biosynthesis
MH  - Dinoprostone/analysis
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/*analysis
MH  - Interferon-gamma/metabolism
MH  - Interleukin-18/*analysis
MH  - Interleukin-18 Receptor alpha Subunit/*analysis
MH  - Monocytes/immunology
MH  - Nitric Oxide Synthase Type II/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Serum/*chemistry
MH  - Synovial Fluid/*chemistry
EDAT- 2009/02/20 09:00
MHDA- 2009/10/10 06:00
CRDT- 2009/02/20 09:00
PHST- 2008/09/02 00:00 [received]
PHST- 2009/01/20 00:00 [accepted]
PHST- 2009/02/20 09:00 [entrez]
PHST- 2009/02/20 09:00 [pubmed]
PHST- 2009/10/10 06:00 [medline]
AID - 10.1007/s10238-009-0036-2 [doi]
PST - ppublish
SO  - Clin Exp Med. 2009 Sep;9(3):215-21. doi: 10.1007/s10238-009-0036-2. Epub 2009 Feb 
      19.