Infectious Triggers and Immune Dynamics in Guillain–Barré Syndrome: Revisiting Campylobacter jejuni and the Silent Role of Haemophilus influenzae

Abstract

Guillain–Barré Syndrome (GBS) is a rapidly progressing immune-mediated neuropathy that remains the leading cause of acute flaccid paralysis worldwide. A substantial proportion of GBS cases are precipitated by infectious agents, most notably Campylobacter jejuni and Haemophilus influenzae, which initiate pathogenic autoimmunity via molecular mimicry. This narrative review aimed to synthesize current evidence on the microbial triggers of GBS and elucidate the immune mechanisms linking infection to neuropathic damage. We discuss the evolving landscape of GBS pathogenesis, emphasizing the roles of ganglioside-like lipooligosaccharide (LOS), host genetic predisposition, and dysregulated immune responses. The clinical heterogeneity of GBS subtypes, including axonal and demyelinating variants, was analyzed in relation to serotype-specific antibody profiles that inform the diagnosis and prognosis. Current therapeutic interventions, including intravenous immunoglobulin and plasma exchange, are critically assessed alongside experimental strategies, such as monoclonal antibody therapies, microbiome modulation, and LOS-targeted vaccines. This review highlights microbial surveillance and precision immunotherapy in the management of GBS. Collectively, this study underscores the central role of microbiological insights in redefining the prevention, diagnosis, and treatment of this complex neuroimmune disorder.