Human Nucleus Pulposis Can Respond to a Pro-inflammatory Stimulus

Burke, John R.; Watson, R. W. G.; Conhyea, D; McCormack, Damien; Dowling, F; Walsh, M. G.; Fitzpatrick, John M.

doi:10.1097/01.brs.0000103341.45133.f3

Cited by 138 publications

(86 citation statements)

References 42 publications

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“…The presence of TNF␣ in herniated disc tissue has long been controversial; while some studies have shown TNF␣ in herniated disc tissue (8,15), others have shown opposite findings (9,10,12,14). Our results indicate that TNF␣ appears transiently in the relatively early stage of IVD-macrophage interaction, suggesting that TNF␣ expression might vary at different stages of herniated disc disease.…”

Section: Discussionmentioning

confidence: 48%

“…TNF␣ is always present in the nucleus pulposus and is thought to induce painrelated behavior in animal models (21,22). High levels of IL-6, IL-8, and PGE 2 are produced in human herniated disc tissue (9,10,12,13,15,19), and their levels show significant correlations with preoperative symptoms of herniated disc disease (8,10,17). However, the mechanisms by which TNF␣, IL-6, IL-8, and PGE 2 contribute to herniated disc disease symptoms, especially sciatica, are unclear.…”

mentioning

confidence: 99%

“…Therefore, inflammation of the herniated disc tissue is thought to be important in the pathologic analysis of herniated disc disease. Herniated disc tissues express a variety of inflammatory factors such as interleukin-1␣ (IL-1␣) (8), IL-1␤ (8), IL-6 (9-15), IL-8 (8)(9)(10)13,16), IL-10 (8), leukotriene B 4 (14), monocyte chemotactic protein 1 (MCP-1) (16), nitric oxide (11,12), prostaglandin E 2 (PGE 2 ) (9,10,15,17,18), RANTES (13), transforming growth factor ␤ (8), thromboxane ␤ 2 (14), and tumor necrosis factor ␣ (TNF␣) (11,12,19,20). Among these, TNF␣, IL-6, IL-8, and PGE 2 have unique pathologic characteristics in herniated disc disease.…”

mentioning

confidence: 99%

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Intervertebral disc and macrophage interaction induces mechanical hyperalgesia and cytokine production in a herniated disc model in rats

Takada¹,

Nishida²,

Maeno³

et al. 2012

Arthritis & Rheumatism

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Objective. The expression of proinflammatory factors such as tumor necrosis factor ␣ (TNF␣), interleukin-6 (IL-6), IL-8, and prostaglandin E 2 (PGE 2 ) is significantly correlated with the symptoms of herniated disc disease. Among the different types of immune cells, macrophages are frequently noted in the herniated disc tissue. We undertook this study to clarify the interaction of the intervertebral disc (IVD) and macrophages with regard to the production of TNF␣, IL-6, IL-8, and PGE 2 .Methods. We developed 2 animal models to assess the interactions of IVDs with macrophages in terms of TNF␣, IL-6, IL-8, and PGE 2 production and painrelated behavior. We also cocultured IVDs and macrophages to assess the role of TNF␣ in IL-6, IL-8, and PGE 2 production.Results. IVD autografts induced TNF␣, IL-6, IL-8, and cyclooxygenase 2 (COX-2) messenger RNA (mRNA) up-regulation; macrophage infiltration was seen shortly after the autograft was implanted. A significant decrease was noted in the mechanical threshold of the ipsilateral paw following the up-regulation of TNF␣,

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Section: Discussionmentioning

confidence: 48%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Intervertebral disc and macrophage interaction induces mechanical hyperalgesia and cytokine production in a herniated disc model in rats

Takada¹,

Nishida²,

Maeno³

et al. 2012

Arthritis & Rheumatism

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“…Le Maitre et al [21] reported that TNF-a and IL-1b are expressed by cells in degenerate intervertebral disc tissues and may be associated with pathogenesis of intervertebral disc degeneration. However, Burke et al [8] found that there is no TNF-a or IL1b secretion by intervertebral disc tissues after stimulation with lipopolysaccharide. We found that IL-6, IL-8, and PGE2 are increased after stimulation with MIF, although TNF-a and IL-1b do not increase.…”

Section: Discussionmentioning

confidence: 99%

Migration Inhibitory Factor Enhances Inflammation via CD74 in Cartilage End Plates with Modic Type 1 Changes on MRI

Xiong

Huang

Cun

et al. 2014

Clinical Orthopaedics &Amp; Related Research

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Background Type 1 Modic changes are characterized by edema, vascularization, and inflammation, which lead to intervertebral disc degeneration. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine closely related to the inflammatory cytokines detected in degenerative intervertebral disc tissues. However, the existence and role of MIF and its receptor CD74 in intervertebral disc degeneration have not been elucidated. Questions/purposes We asked whether (1) MIF and its receptor CD74 are expressed in cartilage end plates with Type 1 Modic changes, (2) MIF is associated with cartilage end plate degeneration, (3) the MIF antagonist (S, R)-3(4-hydroxyphenyl)-4, 5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) suppresses MIF-induced inflammatory cytokine release, and (4) inflammatory cytokines are released by cartilage end plate chondrocytes via CD74 by activating the CD74 antibody (CD74Ab). Methods We examined MIF and CD74 expression by human cartilage end plate chondrocytes and tissues with Type 1 Modic changes from eight patients using immunocytofluorescence and immunohistochemistry. MIF production by the chondrocytes was assessed by ELISA and PCR. We compared cytokine release by chondrocytes treated with MIF in the presence or absence of exogenous ISO-1 by ELISA. Cytokine release by chondrocytes after treatment with CD74Ab was determined by ELISA. Results MIF was expressed in degenerated human cartilage end plate tissues and chondrocytes. Lipopolysaccharide and tumor necrosis factor a (TNF-a) upregulated MIF expression and increased MIF secretion in chondrocytes in a dose-dependent manner. MIF increased the secretion of IL-6, IL-8, and prostaglandin E2 (PGE2) in a dose-dependent manner. ISO-1 reduced the secretion of IL-6, IL-8, and PGE2. CD74Ab activated CD74 and induced release of inflammatory cytokines. Conclusions Chondrocytes in cartilage end plate with Type 1 Modic changes express MIF and its receptor CD74.

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“…(166,167) The latest therapeutic strategies for DD have included some efforts in upregulating the production of key matrix proteins (e.g., aggrecan), or downregulating the catabolic events induced by the proinflammatory cytokines, IL-1 and TNF-a. (109,(168)(169)(170)(171)(172)(173)(174) To deliver these therapeutic agents, some approaches such as protein injection and viral or non-viral gene transfer have been suggested and preclinically tested. (167,(175)(176)(177) The most direct approach to regenerate or repair a degenerated IVD is by injecting anabolic factors.…”

Section: Lbp Pathophysiologymentioning

confidence: 99%

Intervertebral Disc Degeneration and Low Back Pain: Molecular Mechanisms and Stem Cell Therapy

2018

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BACKGROUND: Low back pain (LBP) mostly caused by disc degeneration, reflects to a tremendous of health care system and economy. More knowledge about these underlying pathologies will improve the opportunities that may represent critical therapeutic targets.CONTeNT: Basic research is advancing the understanding of the pathogenesis and management of LBP at the molecular and genetic levels. Cytokines such as matrix metalloproteinases, phospholipase A2, nitric oxide, and tumor necrosis factor-α are thought to contribute to the development of LBP. Mesenchymal stem cells (MSCs) transplant to cartilage-like cells and secrete extracellular matrix and encourage nucleus pulposus (NP) cell activity Abstract R E V I E W A R T I C L Einhibiting NP cell apoptosis, together with some chemical mediators such as cytokines and growth factors become a safe and effective new strategy for intervertebral disc degeneration (IDD) treatment and regeneration.SUMMARy: IDD occurs where there is a loss of homeostatic balance with a predominantly catabolic metabolic profile. A basic understanding of the molecular changes occurring in the degenerating disc is important for practicing clinicians to help them to inform patients to alter lifestyle choices, identify beneficial or harmful supplements, or offer new biologic, genetic, or stem cell therapies.

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Human Nucleus Pulposis Can Respond to a Pro-inflammatory Stimulus

Cited by 138 publications

References 42 publications

Intervertebral disc and macrophage interaction induces mechanical hyperalgesia and cytokine production in a herniated disc model in rats

Intervertebral disc and macrophage interaction induces mechanical hyperalgesia and cytokine production in a herniated disc model in rats

Migration Inhibitory Factor Enhances Inflammation via CD74 in Cartilage End Plates with Modic Type 1 Changes on MRI

Intervertebral Disc Degeneration and Low Back Pain: Molecular Mechanisms and Stem Cell Therapy

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