Neurotrauma and Inflammation: CNS and PNS Responses

Mediators of Inflammation, 2015 · DOI: http://dx.doi.org/10.1155/2015/251204 · Published: March 9, 2015

Regenerative Medicine Neurology Genetics

Simple Explanation

Traumatic injuries to the central or peripheral nervous systems initiate inflammation. Inflammation's role is complex; in the PNS it aids regeneration, but in the CNS, it often hinders recovery. Following CNS injury, neurons and glial cells are destroyed, which triggers molecular signals that amplify the initial damage, leading to an inflammatory response. Conversely, in the PNS, inflammation helps with axon regeneration by activating Schwann cells and macrophages.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review

Key Findings

1
Neutrophils, initially linked to deleterious effects in CNS trauma due to the release of proinflammatory cytokines, may also have proregenerative functions.
2
Macrophages can be polarized into pro- and anti-inflammatory phenotypes (M1 and M2), influencing tissue repair or exacerbating injury in SCI.
3
Galectin-3, involved in myelin phagocytosis, surprisingly showed that its absence accelerated nerve regeneration in Gal-3 ko mice due to increased pro-inflammatory molecule expression.

Research Summary

This review discusses the inflammatory responses after nervous system trauma, comparing CNS and PNS inflammation regarding magnitude, cell types, and effector molecules. In SCI, secondary damage involves hemorrhage, edema, and glial scar formation, hindering regeneration, while the PNS benefits from Schwann cell activation and macrophage involvement. The balance between pro- and anti-inflammatory signals is crucial for axon regeneration, with uncontrolled inflammation leading to nerve pathologies.

Practical Implications

Pharmacological Targets

Identifying precise mechanisms that elicit and maintain inflammation could lead to pharmacological drugs that positively affect tissue regenerative capacity.

Modulating Macrophage Polarization

Therapeutic strategies can be developed to modulate macrophage polarization towards the M2 phenotype to improve functional recovery after SCI.

Controlling Inflammation

Understanding how to control the balance of pro- and anti-inflammatory signals could prevent nerve pathologies and promote successful axon regeneration.

Study Limitations

1
The precise role of inflammation after CNS trauma is still a matter of intense debate.
2
The in vivo dynamics of macrophage polarization after nerve injury is still a matter of intense debate.
3
The precise contribution of galectin-3 to PNS degeneration and regeneration still needs elucidation.

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