PMID- 19560272
OWN - NLM
STAT- MEDLINE
DCOM- 20091117
LR  - 20090831
IS  - 1872-6623 (Electronic)
IS  - 0304-3959 (Linking)
VI  - 145
IP  - 1-2
DP  - 2009 Sep
TI  - Experimental arthritis causes tumor necrosis factor-alpha-dependent infiltration 
      of macrophages into rat dorsal root ganglia which correlates with pain-related 
      behavior.
PG  - 151-9
LID - 10.1016/j.pain.2009.06.002 [doi]
AB  - After peripheral nerve damage macrophages infiltrate the dorsal root ganglia 
      (DRG) in which cell bodies of lesioned neurons are located. However, infiltration 
      of macrophages into the DRGs was also reported in complete Freund's adjuvant 
      (CFA)-induced inflammation raising the question whether CFA inflammation induces 
      nerve cell damage or whether peripheral inflammation may also trigger macrophage 
      infiltration into DRGs. Related questions are, first, which signals trigger 
      macrophage infiltration into DRGs and, second, is macrophage infiltration 
      correlated with pain-related behavior. Using the rat model of unilateral 
      antigen-induced arthritis (AIA) in the knee we found a massive infiltration of 
      ED1(+) macrophages into the ipsi- and contralateral lumbar DRGs but not into 
      thoracic DRGs. At no time point of AIA DRG neurons showed expression of 
      activating transcription factor-3 (ATF3) indicating that macrophage infiltration 
      is not explainable by nerve cell lesions in this model. During AIA, lumbar but 
      not thoracic DRGs exhibited a bilateral de novo expression of vascular cell 
      adhesion molecule-1 (VCAM-1) which is known to be involved in macrophage 
      infiltration. Tumor necrosis factor-alpha (TNF-alpha) neutralization with 
      etanercept or infliximab treatment after induction of AIA significantly reduced 
      both macrophage infiltration and VCAM-1 expression. It also decreased mechanical 
      hyperalgesia at the inflamed joint although the joint inflammation itself was 
      barely attenuated, and it reduced mechanical hyperalgesia at the non-inflamed 
      contralateral knee joint. Thus, bilateral segment-specific infiltration of 
      macrophages into DRGs is part of an unilateral inflammatory process in peripheral 
      tissue and it may be involved in the generation of hyperalgesia in particular on 
      the non-inflamed side.
FAU - Segond von Banchet, Gisela
AU  - Segond von Banchet G
AD  - Institute of Physiology I, University Hospital Jena, Germany. 
      Gisela.SegondvonBanchet@mti.uni-jena.de
FAU - Boettger, Michael K
AU  - Boettger MK
FAU - Fischer, Nadja
AU  - Fischer N
FAU - Gajda, Mieczyslaw
AU  - Gajda M
FAU - Brauer, Rolf
AU  - Brauer R
FAU - Schaible, Hans-Georg
AU  - Schaible HG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090626
PL  - United States
TA  - Pain
JT  - Pain
JID - 7508686
RN  - 0 (Activating Transcription Factor 3)
RN  - 0 (Antibodies)
RN  - 0 (Atf3 protein, rat)
RN  - 0 (Ectodysplasins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 9007-81-2 (Freund's Adjuvant)
SB  - IM
MH  - Activating Transcription Factor 3/metabolism
MH  - Animals
MH  - Antibodies/therapeutic use
MH  - Arthritis, Experimental/chemically induced/*complications/metabolism/pathology
MH  - Disease Models, Animal
MH  - Ectodysplasins/metabolism
MH  - Female
MH  - Freund's Adjuvant/adverse effects
MH  - *Ganglia, Spinal/metabolism/pathology/physiopathology
MH  - Hyperalgesia/*etiology
MH  - Knee Injuries/etiology
MH  - Macrophages/*pathology
MH  - Neutrophil Infiltration/drug effects/physiology
MH  - Pain Threshold/*physiology
MH  - Rats
MH  - Tumor Necrosis Factor-alpha/immunology/*metabolism
MH  - Vascular Cell Adhesion Molecule-1/metabolism
EDAT- 2009/06/30 09:00
MHDA- 2009/11/18 06:00
CRDT- 2009/06/30 09:00
PHST- 2008/11/07 00:00 [received]
PHST- 2009/05/06 00:00 [revised]
PHST- 2009/06/01 00:00 [accepted]
PHST- 2009/06/30 09:00 [entrez]
PHST- 2009/06/30 09:00 [pubmed]
PHST- 2009/11/18 06:00 [medline]
AID - S0304-3959(09)00327-3 [pii]
AID - 10.1016/j.pain.2009.06.002 [doi]
PST - ppublish
SO  - Pain. 2009 Sep;145(1-2):151-9. doi: 10.1016/j.pain.2009.06.002. Epub 2009 Jun 26.