Butyrate alleviates inflammatory response and NF-κB activation in human degenerated intervertebral disc tissues

2020 ◽  
Vol 78 ◽  
pp. 106004 ◽  
Author(s):  
Jialin Jia ◽  
Lin Nie ◽  
Yi Liu
Keyword(s):  
Inflammatory Response ◽  
Intervertebral Disc

Inflammatory response of intervertebral disc cells is reduced by fibrin sealant scaffoldin vitro

2012 ◽  
Vol 8 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Zorica Buser ◽  
Jane Liu ◽  
Kevin J. Thorne ◽  
Dezba Coughlin ◽  
Jeffery C. Lotz
Keyword(s):  
Inflammatory Response ◽  
Intervertebral Disc ◽  
Fibrin Sealant ◽  
Disc Cells

scholarly journals Circ_0004354 might compete with circ_0040039 to induce NPCs death and inflammatory response by targeting miR-345-3p-FAF1/TP73 axis in intervertebral disc degeneration

2022 ◽  
Vol 2022 ◽  
pp. 1-21
Author(s):  
Yongjin Li ◽  
Xiaojing Wu ◽  
Jianhua Li ◽  
Lilong Du ◽  
Xuke Wang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Pathological Process ◽  
Circular Rnas ◽  
Nucleus Pulposus Cells ◽  
Promising Therapeutic Target ◽  
Pathological Mechanism ◽  
Ecm Degradation

The abnormal function of nucleus pulposus cells (NPCs) plays a crucial role in the pathogenesis of intervertebral disc degeneration (IVDD). Recent studies have demonstrated that circular RNAs (circRNAs) are involved in the pathological process of IVDD by regulating NPCs’ function. Nevertheless, the investigation on circRNA-circRNA interaction has not yet been reported. Here, we identified the top upregulated circ_0040039 and circ_0004354 in IVDD, derived from the syntrophin beta 2 gene but had different degrees of biological functions. Accumulating studies have reported PANoptosis is composed of apoptosis, pyroptosis, and necroptosis. Based on this, we think there should be a new pro-inflammatory cell death PAoptosis in the form of apoptosis and pyroptosis. Circ_0004354 might compete with circ_0040039 to induce the development of IVDD by modulating miR-345-3p-FAF1/TP73 axis-mediated PAoptosis, inflammatory response, growth inhibition, and ECM degradation of NPCs. Thus, these findings offer a novel insight into the circRNAs-mediated posttranscriptional regulatory network in IVDD, contributing to further clarification of the pathological mechanism of IVDD to develop a promising therapeutic target for IVDD diseases.

Juvenile Intervertebral Disc Calcification: Recognition, Management, and Pathogenesis

Neurosurgery ◽  
1991 ◽  
Vol 28 (1) ◽  
pp. 130-135 ◽  
Author(s):  
Mark S. Dias ◽  
Dachling Pang
Keyword(s):  
Inflammatory Response ◽  
Neck Pain ◽  
Intervertebral Disc ◽  
Clinical Symptoms ◽  
Intervertebral Discs ◽  
Disc Protrusion ◽  
Intervertebral Disc Calcification ◽  
Neurological Signs ◽  
Erythrocyte Sedimentation ◽  
Compressive Myelopathy

Abstract Juvenile intervertebral disc calcification is an uncommon disorder of childhood, characterized by calcification of the nucleus pulposus of one or more intervertebral discs. Calcification may remain dormant or subsequently become symptomatic. The symptoms include fever, malaise, and neck pain and are associated with an elevated erythrocyte sedimentation rate and, occasionally, leukocytosis. Although disc protrusion occurs in 38% of patients, neurological signs are distinctly uncommon. We report the case of a patient with a herniated T2-T3 calcified intervertebral disc and compressive myelopathy. Juvenile intervertebral disc calcification is generally a self-limiting disease that seldom requires an operation. The symptoms are transient, and resorption of the disc calcification is the rule once symptoms occur. Neither the cause of the disc calcification nor the trigger for the onset of symptoms is known. An inflammatory response within the disc appears to give rise to clinical symptoms and is associated with eventual resorption of the disc calcification.

scholarly journals Modulation of the In Vivo Inflammatory Response by Pro- Versus Anti-Inflammatory Intervertebral Disc Treatments

2020 ◽  
Vol 21 (5) ◽  
pp. 1730 ◽  
Author(s):  
Carla Cunha ◽  
Graciosa Q. Teixeira ◽  
Cláudia Ribeiro-Machado ◽  
Catarina L. Pereira ◽  
Joana R. Ferreira ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Intervertebral Disc ◽  
Immune Cell ◽  
Treated Group ◽  
Hernia Formation ◽  
Injury Model ◽  
Anti Inflammatory ◽  
Ivd Degeneration

Inflammation is central in intervertebral disc (IVD) degeneration/regeneration mechanisms, and its balance is crucial to maintain tissue homeostasis. This work investigates the modulation of local and systemic inflammatory response associated with IVD degeneration/herniation by administration of PRO- versus ANTI-inflammatory treatments. Chitosan/poly-γ-glutamic acid nanocomplexes, known as pro-inflammatory (PRO), and soluble diclofenac, a non-steroidal anti-inflammatory drug (ANTI), were intradiscally administered in a rat IVD injury model, 24 h after lesion. Two weeks after administration, a reduction of disc height accompanied by hernia formation was observed. In the PRO-inflammatory treated group, IL-1β, IL-6 and COX-2 IVD gene expression were upregulated, and loss of nucleus pulposus (NP) structure and composition was observed. Systemically, lower T-cell frequency was observed in the lymph nodes (LN) and spleen (SP) of the PRO group, together with an increase in CD4+ T cells subset in the blood (BL) and LN. In contrast, the ANTI-group had higher proteoglycans/collagen ratio and collagen type 2 content in the NP, while an increase in the frequency of myeloid cells, M1 macrophages and activated macrophages (MHCII+) was observed at the systemic level. Overall, this study illustrates the dynamics of local and systemic inflammatory and immune cell responses associated with intradiscal therapies, which will contribute to designing more successful immunomodulatory treatments for IVD degeneration.

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