PMID- 19567627
OWN - NLM
STAT- MEDLINE
DCOM- 20091008
LR  - 20220409
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 36
IP  - 8
DP  - 2009 Aug
TI  - The tumor necrosis factor-alpha-blocking agent infliximab inhibits interleukin 
      1beta (IL-1beta) and IL-6 gene expression in human osteoblastic cells.
PG  - 1575-9
LID - 10.3899/jrheum.081321 [doi]
AB  - OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine 
      involved in the pathogenesis of several rheumatic diseases, including rheumatoid 
      arthritis (RA), associated with systemic bone loss and subchondral bone erosions. 
      TNF-alpha-blocking agents such as infliximab have been successful in treatment of 
      disease-modifying antirheumatic drug-resistant rheumatic diseases. Infliximab 
      therapy in RA also had beneficial effects on local bone destruction and bone 
      mineral density. We assessed effects of infliximab treatment on the bone tissue 
      compartment and cytokine profile expression in vitro. METHODS: Osteoblast-like 
      cells were exposed for 24 h to sera of RA patients collected at baseline and 
      after 1 month (T1) and 3 years (T2) of infliximab treatment. Total RNA was 
      extracted, and expression of interleukin 1beta (IL-1beta), IL-6, and 
      osteoprotegerin (OPG) was measured by RT-PCR. RESULTS: IL-1beta gene expression 
      was significantly reduced by the T1 serum, and the same decrease was elicited by 
      the T2 serum. IL-6 downregulation was evident with the T2 serum. OPG was 
      unaffected. CONCLUSION: The finding of downregulation of inflammatory cytokines 
      was interesting, particularly IL-6, which plays a crucial role in 
      arthritis-related bone loss due to its involvement in osteoclast recruitment and 
      activation. These results may represent a biological explanation and a link for 
      the clinical observation of the beneficial effects of anti-TNF-alpha agents on 
      the progression of rheumatic diseases at the bone level.
FAU - Musacchio, Estella
AU  - Musacchio E
AD  - Rheumatology Unit, Department of Clinical and Experimental Medicine, University 
      of Padova, Padova, Italy.
FAU - Valvason, Chiara
AU  - Valvason C
FAU - Botsios, Constantin
AU  - Botsios C
FAU - Ostuni, Francesca
AU  - Ostuni F
FAU - Furlan, Antonio
AU  - Furlan A
FAU - Ramonda, Roberta
AU  - Ramonda R
FAU - Modesti, Valentina
AU  - Modesti V
FAU - Sartori, Leonardo
AU  - Sartori L
FAU - Punzi, Leonardo
AU  - Punzi L
LA  - eng
PT  - Journal Article
DEP - 20090630
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Blood Proteins)
RN  - 0 (IL6 protein, human)
RN  - 0 (Interleukin-18)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (Osteoprotegerin)
RN  - 0 (TNFRSF11B protein, human)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - B72HH48FLU (Infliximab)
SB  - IM
MH  - Antibodies, Monoclonal/*therapeutic use
MH  - Antirheumatic Agents/*therapeutic use
MH  - Blood Proteins/pharmacology
MH  - Cell Line
MH  - Gene Expression/drug effects/immunology
MH  - Humans
MH  - In Vitro Techniques
MH  - Infliximab
MH  - Interleukin-18/genetics
MH  - Interleukin-1beta/*genetics
MH  - Interleukin-6/*genetics
MH  - Osteoblasts/cytology/*physiology
MH  - Osteoprotegerin/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Serum
MH  - Tumor Necrosis Factor-alpha/*adverse effects
EDAT- 2009/07/02 09:00
MHDA- 2009/10/09 06:00
CRDT- 2009/07/02 09:00
PHST- 2009/07/02 09:00 [entrez]
PHST- 2009/07/02 09:00 [pubmed]
PHST- 2009/10/09 06:00 [medline]
AID - jrheum.081321 [pii]
AID - 10.3899/jrheum.081321 [doi]
PST - ppublish
SO  - J Rheumatol. 2009 Aug;36(8):1575-9. doi: 10.3899/jrheum.081321. Epub 2009 Jun 30.