Role of inflammation and cytokines in peripheral nerve regeneration
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
24083435
DOI
10.1016/b978-0-12-410499-0.00007-1
PII: B978-0-12-410499-0.00007-1
Knihovny.cz E-resources
- Keywords
- Axonal regeneration, Cytokines, Immune cells, Inflammatory mediators, Neuroinflammation, Wallerian degeneration,
- MeSH
- Cytokines immunology metabolism MeSH
- Humans MeSH
- Peripheral Nerves immunology metabolism MeSH
- Peripheral Nerve Injuries immunology metabolism MeSH
- Nerve Regeneration physiology MeSH
- Signal Transduction physiology MeSH
- Wallerian Degeneration immunology metabolism MeSH
- Inflammation immunology metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Cytokines MeSH
This chapter provides a review of immune reactions involved in classic as well as alternative methods of peripheral nerve regeneration, and mainly with a view to understanding their beneficial effects. Axonal degeneration distal to nerve damage triggers a cascade of inflammatory events alongside injured nerve fibers known as Wallerian degeneration (WD). The early inflammatory reactions of WD comprise the complement system, arachidonic acid metabolites, and inflammatory mediators that are related to myelin fragmentation and activation of Schwann cells. Fine-tuned upregulation of the cytokine/chemokine network by Schwann cells activates resident and hematogenous macrophages to complete the clearance of axonal and myelin debris and stimulate regrowth of axonal sprouts. In addition to local effects, immune reactions of neuronal bodies and glial cells are also implicated in the survival and conditioning of neurons to regenerate severed nerves. Understanding of the cellular and molecular interactions between the immune system and peripheral nerve injury opens new possibilities for targeting inflammatory mediators to improve functional reinnervation.
References provided by Crossref.org
Early inflammatory profiling of schwannoma cells induced by lipopolysaccharide