Intervertebral disc cells produce tumor necrosis factor alpha, interleukin-1beta, and monocyte chemoattractant protein-1 immediately after herniation: an experimental study using a new hernia model.
METHODS
A new hernia model that simulates human disc herniations was developed in rabbits. The herniated discs were examined by gross appearance and histology and production of tumor necrosis factor alpha, interleukin-1beta, and monocyte chemoattractant protein-1 was investigated.


OBJECTIVE
To clarify the early mechanism of spontaneous herniated disc resorption.


BACKGROUND
Macrophage infiltration in herniated discs is essential for disc resorption. However, surgically removed human herniated disc tissues and existing animal hernia models are not suitable for analyzing the mechanism of macrophage infiltration. Recently, we have demonstrated that intervertebral disc cells are capable of producing monocyte chemoattractant protein-1, a potent macrophage chemoattractant, after stimulation with tumor necrosis factor alpha and interleukin-1beta.


METHODS
Intervertebral disc herniations were surgically developed in rabbits using a new technique. The herniated discs were excised at appropriate time intervals after the surgery, and the size and histologic findings were examined. Expressions of tumor necrosis factor alpha, interleukin-1beta, and monocyte chemoattractant protein-1 in herniated discs were investigated immunohistochemically.


RESULTS
A new rabbit model of disc herniation was established. The herniated discs spontaneously reduced in size by 12 weeks postsurgery. Infiltrating cells, mainly composed of macrophages, were observed from day 3. Immunohistochemically, intervertebral disc cells in the herniated discs produced tumor necrosis factor alpha and interleukin-1beta on day 1, followed by monocyte chemoattractant protein-1 on day 3.


CONCLUSIONS
The new hernia model appears to be very useful for studying herniated disc resorption. Intervertebral disc cells may produce inflammatory cytokines/chemokine immediately after the onset of disc herniation, possibly triggering subsequent macrophage infiltration that leads to disc resorption.
Yoshida
Masakazu
M
Department of Orthopaedic Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. seikeigeka-yoshida@kumamotoh.rofuku.go.jp
Nakamura
Takafumi
T
Sei
Akira
A
Kikuchi
Taro
T
Takagi
Katsumasa
K
Matsukawa
Akihiro
A
D000818:Animals; D018932:Chemokine CCL2 / Q000378:metabolism*; D015299:Discitis / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D007375:Interleukin-1 / Q000378:metabolism*; D007403:Intervertebral Disc / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007405:Intervertebral Disc Displacement / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D008264:Macrophages / Q000473:pathology; D009339:Needles; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D014951:Wounds, Stab
D018932:Chemokine CCL2; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha