Immunomodulatory Potential of Aromatic Ginger Against Guillain-Barré Syndrome-Associated Immune Dysregulation

Background: Guillain-Barré Syndrome (GBS) is an acute immune-mediated neuropathy characterized by progressive muscle weakness and peripheral nerve demyelination. A notable increase in GBS cases in India in early 2025 emphasized the need for novel therapeutic interventions. Objective: Medicinal plants of the genus Kaempferia are traditionally recognized for their anti-inflammatory and neuroprotective properties, predominantly studied in rhizomes. However, the aerial parts remain largely underexplored despite sharing a substantial number of volatile constituents. Methods: This study evaluates the neuroprotective and immunomodulatory potential of the aerial parts of Kaempferia parviflora, K. elegans, and K. rotunda through an integrative in silico approach. Pharmacokinetic profiling was conducted using SwissADME, and GBS-associated genes were retrieved from GeneCards. Compound–target interactions (SuperPred) were integrated with protein–protein interaction analyses (STRING, Cytoscape). Key hub proteins were identified, and selected phytocompounds were docked against NFKB1, PI3K, and mTOR using AutoDock 1.5.7, alongside known inhibitors for comparative evaluation. Results: GC–MS analysis identified 91 volatile phytocompounds, of which 42 exhibited favorable ADME properties. Integration of compound–target predictions with GeneCards data revealed 105 overlapping GBS-associated genes, including key regulators of immune and inflammatory pathways. PPI network analysis highlighted NFKB1, PI3K, and mTOR as central hubs. Molecular docking demonstrated strong binding affinities of Kolavelool and 2-Propenoic acid, 3-(2-formyl-4-methoxyphenyl)-, ethyl ester with NFKB1 (–6.5 kcal/mol), PI3K (–7.0 kcal/mol), and mTOR (–6.5 kcal/mol), surpassing standard inhibitors. Conclusion: The study suggests that aerial Kaempferia phytocompounds may modulate NFKB and PI3K/mTOR pathways involved in GBS, highlighting the need for further in vitro and in vivo validation in autoimmune neuroinflammation.