Exploring the Role of Nuclear Factor Kappa B in the Immunobiology of Inflammatory Neuropathies.

BACKGROUND AND

OBJECTIVES

Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are inflammatory conditions, representing prototype examples of immune-mediated disorders of the peripheral nervous system. Activation of the nuclear factor-κB (NF-κB) pathway is crucial for generating immune and inflammatory responses and creating an inflammatory milieu; however, this has not been studied in inflammatory neuropathies. We aimed to quantify the expression levels of two critical genes in the NF-κB pathway ( Nfkb1 and Nfkb2 ), together with a prototype inflammatory gene, Tnfα , in inflammatory neuropathies.

METHODS

Forty-nine patients with inflammatory neuropathies (GBS = 38, CIDP = 11) were recruited prospectively from a single neurology unit. Gene expression levels of Nf κ b1 , Nf κ b2 , and Tnfα were quantified using quantitative real-time polymerase chain reaction.

RESULTS

There were significantly increased expression levels of Nf κ b1 in the inflammatory neuropathy group compared to healthy controls ( P = 0.001), GBS versus healthy controls ( P = 0.03), and CIDP versus healthy controls ( P = 0.003). There were no significant differences in the expression levels of Nf κ b2 and Tnfα genes between cases and controls. There was no correlation between the expression levels of these genes and the clinical severity scores.

CONCLUSIONS

The present study provides evidence for NF-κB pathway activation in inflammatory neuropathies, including both GBS and CIDP, suggesting that this spectrum of disorders may share a common central pathway for immune activation. Thus, the NF-κB pathway plays a critical role in the immunopathogenesis of inflammatory neuropathies; however, the molecular interacting partners within the immune system need to be studied to identify the differential immune trajectories in GBS and CIDP.