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Experimental arthritis causes tumor necrosis factor-alpha-dependent infiltration of macrophages into rat dorsal root ganglia which correlates with pain-related behavior.
Pain. 2009 Sep; 145(1-2):151-9.PAIN

Abstract

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.

Authors+Show Affiliations

Institute of Physiology I, University Hospital Jena, Germany. Gisela.SegondvonBanchet@mti.uni-jena.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19560272

Citation

Segond von Banchet, Gisela, et al. "Experimental Arthritis Causes Tumor Necrosis Factor-alpha-dependent Infiltration of Macrophages Into Rat Dorsal Root Ganglia Which Correlates With Pain-related Behavior." Pain, vol. 145, no. 1-2, 2009, pp. 151-9.
Segond von Banchet G, Boettger MK, Fischer N, et al. Experimental arthritis causes tumor necrosis factor-alpha-dependent infiltration of macrophages into rat dorsal root ganglia which correlates with pain-related behavior. Pain. 2009;145(1-2):151-9.
Segond von Banchet, G., Boettger, M. K., Fischer, N., Gajda, M., Bräuer, R., & Schaible, H. G. (2009). Experimental arthritis causes tumor necrosis factor-alpha-dependent infiltration of macrophages into rat dorsal root ganglia which correlates with pain-related behavior. Pain, 145(1-2), 151-9. https://doi.org/10.1016/j.pain.2009.06.002
Segond von Banchet G, et al. Experimental Arthritis Causes Tumor Necrosis Factor-alpha-dependent Infiltration of Macrophages Into Rat Dorsal Root Ganglia Which Correlates With Pain-related Behavior. Pain. 2009;145(1-2):151-9. PubMed PMID: 19560272.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Experimental arthritis causes tumor necrosis factor-alpha-dependent infiltration of macrophages into rat dorsal root ganglia which correlates with pain-related behavior. AU - Segond von Banchet,Gisela, AU - Boettger,Michael K, AU - Fischer,Nadja, AU - Gajda,Mieczyslaw, AU - Bräuer,Rolf, AU - Schaible,Hans-Georg, Y1 - 2009/06/26/ PY - 2008/11/07/received PY - 2009/05/06/revised PY - 2009/06/01/accepted PY - 2009/6/30/entrez PY - 2009/6/30/pubmed PY - 2009/11/18/medline SP - 151 EP - 9 JF - Pain JO - Pain VL - 145 IS - 1-2 N2 - 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. SN - 1872-6623 UR - https://www.unboundmedicine.com/medline/citation/19560272/Experimental_arthritis_causes_tumor_necrosis_factor_alpha_dependent_infiltration_of_macrophages_into_rat_dorsal_root_ganglia_which_correlates_with_pain_related_behavior_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3959(09)00327-3 DB - PRIME DP - Unbound Medicine ER -