T<sub>reg</sub> cell-mediated clinical response to IVIG therapy in GBS patients was associated with reciprocal regulation of effector T cells-expressing TNF-α.
DSCs showed a significant increase in IL-6 (p < 0.05), TNF-α (p < 0.05), IL-10 (p < 0.01), and TGF-β (p < 0.05) secretion after GBS infection, while these changes were not observed in infected ESCs.
Tumor necrosis factor-α (TNF-α), a proinflammatory cytokine, promotes transendothelial migration by upregulating endothelial expression of inflammatory mediators, including CCL2, a chemokine implicated in GBS.
Subgroup analysis further provided evidence of significant association between TNF-α308 G/A and risk of the GBS in Asian population (GG+GA vs. AA: OR=32, 95%CI=0.11-0.93; GG vs. AA: OR=0.32, 95%CI=0.15-0.68).
Our data suggest that IL-12 promotes disease development in AIDP and in contrast to previously inflammatory assumptions, TNF-alpha may play double roles in GBS.
The MMP9 C(-1562)T and TNFA C(-863)A SNP were associated with severe weakness and poor outcome, indicating that these SNP may be one of the factors predisposing to a severe form of GBS.
Having previously shown that GBS infection impairs cerebral blood flow autoregulation and increases prostaglandin (PG) levels, we examined the regulation of some crucial inflammatory mediators (PGs, nitric oxide (NO), tumor necrosis factor-a) in the brain and cerebral microvessels (MVs) from newborn piglets.
A significantly higher frequency of the 100-base pair (bp) (TNFa2) allele of the TNFa microsatellite marker, which is associated with high TNF alpha production, existed in Campylobacter jejuni-positive (Cj+) GBS patients than in controls, suggesting the involvement of a genetic predisposition to high TNF alpha secretion in the development of C. jejuni-related GBS.