Abstract

OBJECTIVE To delineate the possible implication of the immunosuppressive cytokine transforming growth factor beta 1 (TGF-β1) in the pathogenesis of Guillain-Barré syndrome. Guillain-Barré syndrome is a disorder that may implicate cytokines in its pathogenesis. TGF-β1 is a potent anti-inflammatory cytokine occasionally shown to be regulated in the course of demyelinating disorders.

METHODS The study measured circulating proinflammatory and anti-inflammatory cytokines from the progressing phase to early recovery in patients with Guillain-Barré syndrome. Plasma concentrations of TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-10, and TGF-β1 were prospectively evaluated in 15 patients with Guillain-Barré syndrome every three days for the first 15 days after admission to hospital, and in 15 controls with non-inflammatory neurological diseases.

RESULTS Concentrations of TGF-β1 in plasma were decreased in 13/15 patients (87 %) at day 1, remained low during progression and the plateau of paralysis (days 1–10), and then progressively increased up to control concentrations during early recovery (days 12–15). Concentrations of plasma TGF-β1 correlated positively with motor function, the lowest values being found in the most disabled patients. Concentrations of plasma TGF-β1 were decreased before any treatment, and during treatment by either plasma exchange or intravenous immunoglobulins, plasma exchange being associated with a more pronounced decrease in TGF-β1 at day 7. Circulating TNF-α concentrations were raised, as previously reported, when other cytokines were either randomly increased (IL-2, IL-6), or undetectable (IL-1, IL-4, IL-7, IL-10).

CONCLUSIONS Down regulation of TGF-β1 in the early course of Guillain-Barré syndrome could participate in neural inflammation.