Localization and changes of intraneural inflammatory cytokines and inducible-nitric oxide induced by mechanical compression.
METHODS
Investigation of intraneural inflammation induced by mechanical compression.


OBJECTIVE
In order to investigate the mechanism of neuropathy, this study used a median nerve compression model in dogs. Immunohistochemistry was used to examine the localization and changes of inflammatory cytokines and nitric oxide (NO).


BACKGROUND
The manifestation of pain at sites of inflammation has a close relationship with the release of mediators from macrophages such as interleulin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha), as well as with NO. However, the mediators involved in inflammation of nerve due to mechanical compression remain almost unknown.


METHODS
In this study, the median nerve of dogs was compressed with a clip for three weeks to observe the changes caused by compression. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against IL-1beta, TNF-alpha, and inducible nitric oxide synthesis (i-NOS) were used to examine the localization and changes of these mediators caused by nerve compression.


RESULTS
In control animals, resident T cells were detected, but there were no macrophages. IL-1beta was positive in the Schwann cells and vascular endothelial cells. However, no cells showed TNF-alpha or i-NOS positively. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for IL-1beta, TNF-alpha and i-NOS.


CONCLUSIONS
Inflammatory cytokines and NO may be involved in intraneural inflammatory changes arising from mechanical compression. Such mediators may be of importance in the manifestation of neuropathy.
Kobayashi
Shigeru
S
Department of Orthopaedics and Rehabilitation Medicine, School of Medicine, Fukui Medical University, Shimoaizuki 23, Matsuoka, Fukui 910-1193, Japan. kshigeru@fmsrsa.fukui-med.ac.jp
Baba
Hisatoshi
H
Uchida
Kenzo
K
Shimada
Seiichiro
S
Negoro
Kouhei
K
Takeno
Kenichi
K
Yayama
Takafumi
T
Yamada
Shuichi
S
Yoshizawa
Hidezo
H
D000818:Animals; D004285:Dogs; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000378:metabolism*; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D008475:Median Nerve / Q000276:immunology / Q000378:metabolism / Q000648:ultrastructure; D020423:Median Neuropathy / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D046529:Microscopy, Electron, Transmission; D009186:Myelin Sheath / Q000276:immunology / Q000378:metabolism / Q000648:ultrastructure; D009408:Nerve Compression Syndromes / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D014855:Wallerian Degeneration / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology
D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II