Biomarkers of Guillain-Barré Syndrome: Some Recent Progress, More Still to Be Explored

Abstract

Guillain-Barré syndrome (GBS), the axonal subtype of which is mainly triggered by C. jejuni with ganglioside-mimicking lipooligosaccharides (LOS), is an immune-mediated disorder in the peripheral nervous system (PNS) accompanied by the disruption of the blood-nerve barrier (BNB) and the blood-cerebrospinal fluid barrier (B-CSF-B). Biomarkers of GBS have been extensively explored and some of them are proved to assist in the clinical diagnosis and in monitoring disease progression as well as in assessing the efficacy of immunotherapy. Herein, we systemically review the literature on biomarkers of GBS, including infection-/immune-/BNB, B-CSF-B, and PNS damage-associated biomarkers, aiming at providing an overview of GBS biomarkers and guiding further investigations. Furthermore, we point out further directions for studies on GBS biomarkers.

Figure 1

Axonal damage type of GBS is triggered by a subset of C. jejuni containing ganglioside-mimicking LOS on outer membrane. Immune response to C. jejuni induces the unbalance of Th1/Th2/Th17/Treg and cytokines that is crucial for the development of GBS. Chemokines are responsible for the infiltration of immune cells and complements activated by antibodies could mediate PNS lesion. Damage of barriers and PNS permits CSF to serve as an important source of biomarkers. Structural molecules of PNS, including myelin sheath molecules and neuron molecules, are released to CSF due to the damage of PNS and may provoke further immune response. Disturbance of BNB also results in an alteration of protein content in CSF due to blood protein influx.