mRNA Expression of Cytokines and Chemokines in Herniated Lumbar Intervertebral Discs

Ahn, Sungjin; Cho, Yoon-Woo; Ahn, Myun-Whan; Jang, Sung-Ho; Sohn, Yoon-Kyung; Kim, Hee-Sun

doi:10.1097/00007632-200205010-00005

Cited by 228 publications

(162 citation statements)

References 44 publications

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“…Furthermore, we found that IL-8 increased more than IL-6 and PGE2 in response to inflammatory stimulus, and IL-8 showed a similar trend as those reported by Kim et al [18]. IL-8 is a chemoattractant for lymphocytes and neutrophils [4,5], present in significant concentrations in intervertebral disc tissues [1]. Therefore, our data suggest that IL-8 may play an important role in MIFinduced inflammation and warrants further investigation.…”

Section: Discussionsupporting

confidence: 87%

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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Section: Discussionsupporting

confidence: 87%

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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“…2 There has been much evidence showing that inflammatory factors may play an important role in the etiology of LBP. 1,10,15,22 Increasing polymorphisms in gene encoding for these factors have been reported in lumbar disc diseases and LBP, and, in particular, the SNP of IL-1b may confer susceptibility to LBP. 11,18,20,25 Caspase-9 is an initiator caspase protease for apoptosis, and recent studies have indicated that it plays a significant role in apoptosis in human intervertebral disc degeneration.…”

Section: ©Aans 2013mentioning

confidence: 99%

Analysis of association between IL-1β, CASP-9, and GDF5 variants and low-back pain in Chinese male soldiers

Zuo³

et al. 2013

SPI

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Object Recent studies have suggested that genetic risk factors play an important role in the occurrence of low-back pain (LBP) and lumbar disc disease. The authors' study aimed to assess the association between 3 single-nucleotide polymorphisms (SNPs) and susceptibility to LBP related to military training. Methods In this case-control study, data from 892 Chinese male soldiers were retrospectively reviewed. The case group was made up of 305 soldiers with LBP related to military training and a control group of 587 soldiers without constant LBP for more than 2 weeks. Genomic DNA was extracted from peripheral blood leukocytes of all subjects and polymerase chain reaction products were genotyped. Results No association was found between the SNP of interleukin-1β (IL-1β; +3954C/T) and LBP at both the genotypic (p = 0.104) and the allelic (p = 0.098) level. However, the G allele of caspase-9 (CASP-9) and the T allele of growth differentiation factor 5 (GDF5) were more common in patients with LBP than in patients without LBP (p < 0.001). Conclusions The findings in a Chinese military cohort indicated that CASP-9 (−1263A/G) and GDF5 (+104T/C) polymorphisms are associated with a susceptibility to LBP related to military training.

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“…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%

“…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%

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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mRNA Expression of Cytokines and Chemokines in Herniated Lumbar Intervertebral Discs

Cited by 228 publications

References 44 publications

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

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

Analysis of association between IL-1β, CASP-9, and GDF5 variants and low-back pain in Chinese male soldiers

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

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