Role of Inflammation and Cytokines in Peripheral Nerve Regeneration

Investor logo
Investor logo

Warning

This publication doesn't include Faculty of Economics and Administration. It includes Faculty of Medicine. Official publication website can be found on muni.cz.
Authors

DUBOVÝ Petr JANČÁLEK Radim KUBEK Tomáš

Year of publication 2013
Type Article in Periodical
Magazine / Source International Review of Neurobiology
MU Faculty or unit

Faculty of Medicine

Citation
web http://www.sciencedirect.com/science/article/pii/B9780124104990000071
Doi http://dx.doi.org/10.1016/B978-0-12-410499-0.00007-1
Field Neurology, neurosurgery, neurosciences
Keywords Wallerian degeneration; Neuroinflammation; Immune cells; Inflammatory mediators; Cytokines; Axonal regeneration
Attached files
Description This work 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.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.