Exploring the role of altered oxi-inflammasome activity in the immunobiology of inflammatory neuropathies.

OBJECTIVES

Inflammasome plays a significant role in inflammatory responses. The role of inflammasome and its interactions with oxidative stress markers has not been examined in inflammatory neuropathies like Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). This study aims to explore the roles of inflammasome and oxidative stress pathways in inflammatory neuropathies.

METHODS

This case-controlled study comprised patients with inflammatory neuropathies (n = 60, GBS = 44, CIDP = 16) and age- and gender-matched healthy controls (n = 60). The expressions of inflammasome-related genes (Nlrp3, Casp1, and Il1b) were quantified along with the plasma levels of malondialdehyde (MDA), the end product of lipid peroxidation in all study participants.

RESULTS

The expressions of Nlrp3 (p = 0.0083) and Casp1 (p = 0.0007) genes were significantly up-regulated in GBS patients compared to controls. The plasma MDA levels were also markedly higher in GBS patients than in controls (p = 0.029). The gene expression levels of Nlrp3, Casp1, and Il1b and plasma MDA levels were comparable between CIDP patients and healthy controls. There were no correlations between the expressions of the studied genes and MDA levels with the clinical scores of GBS.

CONCLUSION

The up-regulated expression of Nlrp3 and Casp1 genes and increased levels of MDA suggest the presence of an activated oxi-inflammatory pathway in GBS. These findings provide a new dimension to the current understanding of the immuno-pathogenesis of GBS.