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Alexandre Faisant, Sandra Carignon, Arnaud Menuet, Nicolas Riteau, Marc Le Bert
Posted on Thursday February 29, 2024
DOI: 10.60675/b30k-ht75/sn001-2024/fc3r-short-notes 
This study aimed to establish an experimental model of Guillain-Barré Syndrome (GBS), a peripheral inflammatory neuropathy in humans, using the Experimental Autoimmune Neuritis (EAN) model in C57BL/6 mice. This approach was informed by a comprehensive bibliographic analysis. While this experimental model has been developed successfully in rabbits, rats, and the SJL mouse strain, the literature on its application in C57BL/6 mice is limited. Our protocol analysis encompassed twenty-one articles utilizing the P0180-199 neurogenic peptide to induce EAN in this genetic background. Based on this literature, we selected one protocol for replication and made three adaptations. Despite using high-quality P0(180-199) peptide, we were unable to reproduce the selected EAN protocol or induce any pathological signs, even under optimized conditions. As a control to validate our reagents and methodology, we replicated a different model of inflammatory neuropathy targeting the central nervous system: the well-established Experimental Autoimmune Encephalitis (EAE) protocol. This replication was successful using the same C57BL/6 mouse genetic background and reagents, with the sole exception of the neurogenic peptide employed (MOG(35-55)).