Mechanism and Potential Treatment of Guillain Barr Syndrome and Related Neuropathy
Abstract
Guillain-Barre Syndrome (GBS) encompasses a group of polyneuropathies of high medical importance that affect the peripheralnervous system (PNS) and can extend to the central nervous system (CNS). This study uses a nonhuman primate (NHP) system we established that results in neuroinflammation. We think the system is likely to recapitulate facets of GBS in adults. In this model, neuroinflammation is triggered by infection with Zika virus (ZIKV). A hallmark of neuroinflammation in these animals is consistent acute and chronic neural upregulation of the chemokine CXCL12. We hypothesize that CXCL12 plays dual roles in neuroinflammation. Since CXCL12 regulates lymphocyte migration into the neural parenchyma, it is likely that this chemokine contributes to early inflammation. GBS involves demyelination and CXCL12 is a key chemokine that facilitates myelin repair. Hence, it is likely that CXCL12 also functions positively in myelin repair in the chronic phase. Regulation by CXCL12 is mediated through interaction with its primary cell-surface receptor, CXCR4. Stimulation of CXCR4 by CXCL12 results in activation of multiple signal transduction pathways leading to the migration of CXCR4+ cells. Multiple mechanisms regulate this central CXCL12-CXCR4 axis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Feb 01, 2022
- Accession Number
- AD1171250
Entities
People
- Antonito T Panganiban
Organizations
- Tulane University of Louisiana