PMID- 18484150
OWN - NLM
STAT- MEDLINE
DCOM- 20090331
LR  - 20211020
IS  - 0770-3198 (Print)
IS  - 0770-3198 (Linking)
VI  - 27
IP  - 10
DP  - 2008 Oct
TI  - BDNF in RA: downregulated in plasma following anti-TNF treatment but no 
      correlation with inflammatory parameters.
PG  - 1289-97
LID - 10.1007/s10067-008-0910-4 [doi]
AB  - The involvement of brain-derived neurotrophic factor (BDNF) in rheumatoid 
      arthritis (RA) is largely unknown. The distribution of BDNF and its associated 
      receptors, TrkB and p75, in the synovial tissue of patients with RA was examined 
      and contrasted with that in patients with osteoarthritis (OA). Additionally, 
      levels of BDNF in both synovial tissue and synovial fluid were measured. 
      Furthermore, the effects of anti-tumour necrosis factor (anti-TNF; infliximab) 
      treatment on BDNF levels in the plasma of RA patients were analysed. Cells in the 
      synovium showed immunoreactivity for BDNF and BDNF-, p75- and TrkB-receptor 
      immunoreactions were seen in nerve fibres of nerve fascicles and in association 
      with sensory corpuscles. The levels of BDNF in synovial tissue were not 
      correlated with the number of inflammatory cells observed microscopically or with 
      levels of TNFalpha. Nor did the BDNF levels in synovial fluid correlate with 
      erythrocyte sedimentation rate (ESR) or white blood cell counts. Anti-TNF 
      treatment lead to a decrease in plasma levels of BDNF 14 weeks after the 
      initiation of anti-TNF therapy, i.e., 8 weeks after the last infusion. Higher 
      levels of BDNF were observed in RA patients at baseline compared with those for 
      healthy individuals. However, the levels of BDNF in plasma of patients treated 
      with anti-TNF did not correlate with the changes in ESR or a disease activity 
      score. The clinical significance of this study is that anti-TNF treatment 
      influences plasma levels of BDNF although there was no evidence that BDNF levels 
      correlate with inflammatory parameters in either infliximab-treated or 
      non-infliximab-treated patients with RA. Instead it is likely that sources other 
      than inflammatory cells, including nerve structures, are important sources of 
      BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to 
      effects on circulating and various local cells and/or BDNF-containing neurons.
FAU - Grimsholm, Ola
AU  - Grimsholm O
AD  - Department of Integrative Medical Biology, Section for Anatomy, Umea University, 
      Umea, Sweden. ola.grimsholm@anatomy.umu.se
FAU - Rantapaa-Dahlqvist, Solbritt
AU  - Rantapaa-Dahlqvist S
FAU - Dalen, Tore
AU  - Dalen T
FAU - Forsgren, Sture
AU  - Forsgren S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080517
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - B72HH48FLU (Infliximab)
SB  - IM
MH  - Antibodies, Monoclonal/*therapeutic use
MH  - Arthritis, Rheumatoid/*blood/*drug therapy/immunology
MH  - Blood Sedimentation
MH  - Brain-Derived Neurotrophic Factor/*blood
MH  - Case-Control Studies
MH  - Down-Regulation
MH  - Humans
MH  - Infliximab
MH  - Osteoarthritis, Knee/blood
MH  - Severity of Illness Index
MH  - Synovial Fluid/chemistry
MH  - Synovial Membrane/immunology/metabolism
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
EDAT- 2008/05/20 09:00
MHDA- 2009/04/01 09:00
CRDT- 2008/05/20 09:00
PHST- 2008/01/16 00:00 [received]
PHST- 2008/04/16 00:00 [accepted]
PHST- 2008/04/11 00:00 [revised]
PHST- 2008/05/20 09:00 [pubmed]
PHST- 2009/04/01 09:00 [medline]
PHST- 2008/05/20 09:00 [entrez]
AID - 10.1007/s10067-008-0910-4 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2008 Oct;27(10):1289-97. doi: 10.1007/s10067-008-0910-4. Epub 
      2008 May 17.