Tumour necrosis factor-α has few morphological effects within the dorsal columns of the spinal cord, in contrast to its effects in the peripheral nervous system

Hall, SM; Redford, EJ; Smith, Kenneth J.

doi:10.1016/s0165-5728(00)00213-7

Cited by 24 publications

(8 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…26 TNF-␣ also causes selective cytotoxic damage to Schwann cells and myelin sheaths. 24,67 This inflammatory mediator could, short of inciting tissue damage, cause physiological changes by interfering with impulse propagation through changes in ionic channel expression. 8 Clinically, a pro-inflammatory role for TNF-␣ is supported by an elevated serum level in 27%-63% of patients with GBS, in 25%-57% of patients with chronic inflammatory demyelinating polyneuropathy (CIDP), and in 68% of patients with multifocal motor neuropathy (MMN).…”

Section: Tnf-␣ In Inflammatory Neuropathiesmentioning

confidence: 99%

Tumor necrosis factor‐α antagonists and neuropathy

2007

View full text Add to dashboard Cite

Tumor necrosis factor (TNF)-alpha plays an important role in many aspects of immune system development, immune-response regulation, and T-cell-mediated tissue injury. The evidence that TNF-alpha, released by autoreactive T cells and macrophages, may contribute to the pathogenesis of immune-mediated demyelinating neuropathies is reviewed. TNF-alpha antagonists (infliximab, etanercept, adalimumab) are indicated for the treatment of advanced inflammatory rheumatic and bowel disease, but these drugs can induce a range of autoimmune diseases that also attack the central and peripheral nervous systems. Case histories and series report on the association between anti-TNF-alpha treatment and various disorders of peripheral nerve such as Guillain-Barré syndrome, Miller Fisher syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy with conduction block, mononeuropathy multiplex, and axonal sensorimotor polyneuropathies. The proposed pathogeneses of TNF-alpha-associated neuropathies include both a T-cell and humoral immune attack against peripheral nerve myelin, vasculitis-induced nerve ischemia, and inhibition of signaling support for axons. Most neuropathies improve over a period of months by withdrawal of the TNF-alpha antagonist, with or without additional immune-modulating treatment. Preliminary observations suggest that TNF-alpha antagonists may be useful as an antigen-nonspecific treatment approach to immune-mediated neuropathies in patients with a poor response to, or intolerance of, standard therapies, but further studies are required.

show abstract

Section: Tnf-␣ In Inflammatory Neuropathiesmentioning

confidence: 99%

Tumor necrosis factor‐α antagonists and neuropathy

2007

View full text Add to dashboard Cite

show abstract

“…In spite of these positive results, the early growth of axons along hollow nerve guides is delayed since the conduit's lumen should first be colonized by connective tissue and Schwann cells migrating from the distal nerve stump [3,4]. To prevent this occurrence, a luminal filler must be used for providing a substrate for early nerve fiber regeneration [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Peripheral Nerve Reconstruction Using Enriched Chitosan Conduits

Rochkind¹,

Mandelbaum-Livnat²,

StefaniaRaimondo³

et al. 2017

Scaffolds in Tissue Engineering - Materials, Technologies and Clinical Applications

View full text Add to dashboard Cite

The repair of peripheral nerve traumatic lesions still represents a major cause of permanent motor and sensory impairment. In case of substance loss, a nerve guide should be used to bridge the proximal with the distal stump of the severed nerve. The effectiveness of hollow nerve guides is limited by the delay of axonal growth due to the absence of a regeneration substrate inside the conduit. To fasten up nerve regeneration, nerve guides should thus be enriched by a luminal filler. In this study, we investigated, in a 12-mm rat sciatic nerve defect experimental model, the effectiveness of chitosan-based conduits of different acetylation filled either with a hyaluronic acid gel (NVR gel) or with a magnetic fibrin hydrogel, in comparison with traditional autografts. Results showed that all types of artificial nerve conduits led to functional recovery not significantly different from autografts. By contrast, morphological and morphometrical analyses showed that the best results among nerve guides were found in medium degree of acetylation (DAII: ∼5%) chitosan conduits enriched with the NVR gel.

show abstract

“…TNF-␣ , for example, participates in blood-nerve barrier disruption, endoneurial edema, axonal degeneration and perivascular demyelination [11,12] . TNF-␣ also stimulates the expression of the inducible form of the enzyme nitric oxide synthase (iNOS) [13] , which synthesizes large amounts of nitric oxide (NO) over prolonged periods, contributing to tissue destruction in inflammatory diseases [14,15] .…”

Section: Introductionmentioning

confidence: 99%

Distribution of Inducible Nitric Oxide Synthase and Tumor Necrosis Factor-α in the Peripheral Nervous System of Lewis Rats during Ascending Paresis and Spontaneous Recovery from Experimental Autoimmune Neuritis

Hoz

Castro²,

Santos

et al. 2009

Neuroimmunomodulation

View full text Add to dashboard Cite

Background: Inducible nitric oxide synthase (iNOS) and tumor necrosis factor-α (TNF-α) are pleiotropic molecules with widespread action in autoimmune diseases. Objective: This study characterizes the distribution of iNOS and TNF-α in the spinal nerve roots, dorsal root ganglia and sciatic nerve of Lewis rats during experimental autoimmune neuritis (EAN). Methods: Macrophages and neutrophils were identified by immunofluorescence as cellular sources of iNOS and TNF-α at various stages of EAN induced by synthetic peptide 26. Results: As the disease progressed, iNOS- and TNF-α-bearing cells gradually infiltrated the cauda equina, dorsal root ganglia, Th12–L3 spinal roots, and the sciatic nerve. A severer EAN profile developed when more iNOS- and TNF-α-bearing cells were present, and the recovery from EAN was related to the disappearance of these cells and the regeneration of nerve fibers. Conclusions: This is the first report to show iNOS- and TNF-α-immunoreactive cells in dorsal root ganglia during EAN, suggesting an underlying pathology for the neuropathic pain behavior in EAN. Our results suggest that the cells bearing iNOS and TNF-α in the different parts of the peripheral nervous system are involved in the development of the clinical signs observed at each stage of EAN.

show abstract

Tumour necrosis factor-α has few morphological effects within the dorsal columns of the spinal cord, in contrast to its effects in the peripheral nervous system

Cited by 24 publications

References 53 publications

Tumor necrosis factor‐α antagonists and neuropathy

Tumor necrosis factor‐α antagonists and neuropathy

Peripheral Nerve Reconstruction Using Enriched Chitosan Conduits

Distribution of Inducible Nitric Oxide Synthase and Tumor Necrosis Factor-α in the Peripheral Nervous System of Lewis Rats during Ascending Paresis and Spontaneous Recovery from Experimental Autoimmune Neuritis

Contact Info

Product

Resources

About